Liver

These ingredients are often used in alternative medicine to support liver.

• acaciaScientific

  Acacia gum has demonstrated hepatoprotective effects in human trials: a Phase II trial in RA patients (30 g/day, 12 weeks) significantly reduced liver enzymes and improved albumin levels. Systematic review of clinical trials confirms GA increases hepatic antioxidant enzyme activity (SOD, catalase, glutathione peroxidase) and reduces hepatic oxidative stress.

• acai berryScientific

  Preclinical evidence is robust for acai's hepatoprotective effects, showing it attenuates NAFLD-related liver damage, reduces hepatic oxidative stress, and modulates lipid metabolism in animal models. Traditional Amazonian and Peruvian medicine uses acai root preparations for liver and jaundice conditions. Human clinical trials specifically targeting liver endpoints are lacking.

• activated charcoalScientific

  Activated charcoal interrupts enterohepatic bile acid recirculation by binding bile acids in the intestinal lumen, which compels the liver to upregulate cholesterol-to-bile-acid synthesis (CYP7A1) to maintain the bile acid pool. This hepatic compensatory response is the primary mechanism behind AC's LDL-lowering effect in clinical trials. Preclinical data in mice further show AC increases hepatic expression of both CYP7A1 and HMG-CoA reductase.

• adzuki beanScientific

  Adzuki bean extracts protect against chemically induced hepatotoxicity in rats by upregulating glutathione-linked antioxidant enzymes. Multiple HFD animal studies show adzuki bean reduces hepatic steatosis, ALT, and AST. A 2025 lipidomics study demonstrates adzuki bean flavonoids normalize hepatic lipid profiles and reduce ceramide-linked fibrosis markers.

• agrimonyScientific

  Agrimony has the strongest human clinical evidence of any body system in a 2018 randomised double-blind placebo-controlled trial showing significant reduction in ALT and AST in subjects with elevated liver enzymes. Traditional use for liver conditions is also extensively documented across European folk medicine.

• ajwainScientific

  Hepatoprotective activity is a consistently documented property of ajwain extract in animal studies, including approximately 80% protection against lethal paracetamol doses in rodents. A key 2005 Journal of Ethnopharmacology study specifically characterized hepatoprotective activity. Traditional use as a liver stimulant supports this.

• AKG (alpha-ketoglutarate)Scientific

  AKG protects against hyperlipidemia-induced hepatic lipid accumulation, mitochondrial dysfunction, and oxidative stress via the AMPK-PGC-1α/Nrf2 pathway in animal models. It reduces liver gluconeogenesis and plasma lipid levels. AKG also activates hepatic detoxification (PXR) pathways and reduces LPS-induced liver damage. These effects are currently demonstrated in animal and cell models without direct human RCT confirmation.

• akkermansia muciniphilaScientific

  A. muciniphila consistently reduces hepatic steatosis, liver enzyme levels (ALT/AST), and hepatic inflammation in animal models of NAFLD/NASH, operating via the gut-liver axis by limiting LPS translocation through the portal vein. The 2019 human RCT documented reduced blood markers of liver dysfunction with pasteurized A. muciniphila. A 2025 systematic review of 13 NAFLD mouse model studies confirmed consistent hepatoprotective effects, though human clinical NAFLD trials have not yet been completed.

• ALA (alpha-lipoic acid)Scientific

  Alpha-lipoic acid (ALA) has been studied in multiple human clinical trials for liver-related conditions, particularly non-alcoholic fatty liver disease (NAFLD). Its primary hepatic mechanisms involve antioxidant activity, suppression of inflammatory signaling (NF-κB, TNF-α), improvement of insulin sensitivity, and upregulation of the Nrf2 cytoprotective pathway. Human trial results are mixed: metabolic markers (insulin resistance, adiponectin) improve more consistently than liver enzyme levels or steatosis grade. ALA has not been linked to hepatotoxicity in clinical use.

• alfalfaScientific

  Alfalfa's antioxidant and anti-inflammatory phytochemicals have demonstrated hepatoprotective effects in multiple animal studies, reducing liver enzyme elevations, lipid peroxidation, pro-inflammatory cytokines, and histological liver damage. Mechanistically, liver is the central organ for alfalfa's cholesterol-modulating activity.

• alkanetScientific

  Alkanet root contains pyrrolizidine alkaloids (PAs) that are scientifically documented hepatotoxins. PA metabolites activated by CYP450 enzymes form reactive pyrrole-protein adducts that damage hepatic sinusoidal endothelial cells. Drugs.com and WebMD both warn of risk of acute liver failure and cirrhosis from oral use.

• almondScientific

  A registered RCT in coronary artery disease patients found that almond consumption protected liver enzymes, suggesting hepatoprotective effects. Almonds' antioxidant and anti-inflammatory properties are proposed as the mechanism. Their effect on reducing lipid absorption and improving cardiometabolic parameters also indirectly reduces hepatic lipid burden.

• aloe veraScientific

  Aloe vera is considered hepatoprotective in preclinical research. Animal studies show it attenuates acetaminophen-induced hepatotoxicity by reducing oxidative stress, restoring glutathione, and improving liver histopathology. Aloe vera extract also significantly reduced serum ALT in toxicity models. A human study examined aloe vera juice effects on liver enzymes in a healthy population.

• alpha-caroteneScientific

  Multiple cross-sectional and prospective cohort studies find serum alpha-carotene inversely associated with non-alcoholic fatty liver disease (NAFLD/MAFLD) prevalence and related mortality. A Chinese cross-sectional study (N=2,935) found serum alpha-carotene's highest quartile associated with an OR of 0.44 (95% CI 0.35–0.56) for NAFLD. A NHANES-based US cohort confirmed that higher intake and serum levels of alpha-carotene are associated with lower odds of NAFLD.

• alpha-glycosyl isoquercitrinScientific

  Isoquercitrin (AGIQ's precursor/metabolite) demonstrates hepatoprotective activity via AMPK/YAP pathway activation in hepatocyte models, reducing ROS and apoptosis. Animal studies show AGIQ suppresses hepatic preneoplastic lesion development. The 2022 MDPI EMIQ review and multiple preclinical publications list hepatoprotection as a documented AGIQ pharmacological property.

• alpinia galangalScientific

  ACA from A. galanga significantly elevated hepatic glutathione S-transferase (GST) activity in mice, supporting liver detoxification capacity. Animal studies confirm antioxidant hepatoprotection. Galangin has shown hepatoprotective potential by reducing fibrosis markers in early-stage experiments.

• andrographisScientific

  Andrographis paniculata has deep traditional roots in Ayurveda and Traditional Chinese Medicine as a liver tonic and treatment for jaundice. Its primary bioactive compound, andrographolide, has demonstrated hepatoprotective, anti-inflammatory, antioxidant, and antifibrotic effects across multiple preclinical models. While robust, large-scale human clinical trials specifically for liver disease remain limited, preclinical and observational evidence is substantial, and at least one human cross-sectional study has examined its effect on liver enzymes (ALT) in real-world settings.

• andrographolideScientific

  Andrographolide, the principal diterpenoid lactone from Andrographis paniculata, has well-documented hepatoprotective activity supported by multiple preclinical studies and a growing body of mechanistic research. It reduces oxidative stress, inflammation, and fibrosis in the liver by modulating NF-κB, Nrf2/HO-1, NLRP3, and TGF-β1/Smad2 signaling pathways. Traditional use of the parent plant for liver disorders in Ayurveda, TCM, and Southeast Asian medicine predates modern science. Direct human clinical trials specific to liver disease remain limited, placing most strong evidence at the preclinical level.

• annattoScientific

  Annatto delta-tocotrienol has been evaluated in multiple randomized clinical trials in NAFLD patients, demonstrating reductions in liver enzymes, fatty liver index, hepatic steatosis grade, and HOMA-IR. A 2023 systematic review of 12 studies (4 human) confirmed tocotrienols from palm and annatto improve NAFLD outcomes. Traditional use of annatto leaves for liver disease and hepatitis is also documented.

• appleScientific

  Apple polyphenols modulate hepatic lipid metabolism and have shown hepatoprotective effects in preclinical models. Quercetin is well-documented for hepatoprotective properties. Apple pectin reduces hepatic cholesterol synthesis by promoting bile acid excretion. Animal studies with apple polyphenols show reduced liver fat and inflammation.

• apple cider vinegarScientific

  Animal studies demonstrate ACV mitigates high-fat-diet-induced hepatic steatosis, reducing serum ALT, AST, and hepatic fat vacuoles via gut-liver axis remodeling. ACV polyphenols show hepatoprotective antioxidant activity. No human RCTs with liver endpoints (ALT, AST, steatosis) as primary outcomes have been published.

• arginine alpha ketoglutarateScientific

  AAKG undergoes extensive hepatic metabolism and has documented clinical evidence for enhancing liver detoxification capacity. A 1977 study in liver-cirrhosis patients showed AAKG administration significantly reduced plasma ammonia and serum phenols, indicating improved hepatic oxidative decomposition. The liver also converts arginine to AKG as an energy source.

• aronia melanocarpaScientific

  Aronia melanocarpa protects the liver via antioxidant, anti-inflammatory, and lipid metabolism–modulating mechanisms documented in multiple animal models and a human pilot trial. The Nrf2 signaling pathway, PPARγ downregulation, and gut microbiota modulation are key mechanisms. A 6-week human pilot RCT showed reductions in liver enzyme ALAT.

• artichokeScientific

  Artichoke leaf extract (ALE), derived from Cynara scolymus, has documented hepatoprotective activity supported by both preclinical studies and human clinical trials. Key mechanisms include antioxidant action, anti-inflammatory effects via suppression of the NF-κB/TLR4 pathway, and choleretic (bile-stimulating) properties. A randomized, double-blind, placebo-controlled trial in NASH patients demonstrated significant improvement in liver enzymes (ALT/AST) and lipid profiles. Regulatory bodies such as EMA/ESCOP recognize traditional use of artichoke leaf for biliary/digestive support, and emerging clinical data extend this to metabolic liver disease contexts.

• ashitabaScientific

  Ashitaba has one small human RCT demonstrating improvement in liver function markers in alcohol drinkers. Animal studies confirm hepatoprotective effects against bile duct ligation injury and fatty liver. A metabolic syndrome pilot confirmed hepatoprotective efficacy. AMPK activation in liver suppresses lipogenesis and fat accumulation.

• astaxanthinScientific

  Astaxanthin, a xanthophyll carotenoid from marine organisms, has documented preclinical evidence for hepatoprotection via antioxidant, anti-inflammatory, and lipid-regulating mechanisms across conditions including NAFLD, liver fibrosis, and drug-induced liver injury. Human clinical data are emerging but limited: RCTs have shown improvements in oxidative stress biomarkers in overweight adults, and a meta-analysis of RCTs found a modest but statistically significant increase in ALT without meaningful changes to other liver enzymes. Reviewers consistently note that robust, liver-disease-specific human trials remain insufficient to confirm clinical efficacy.

• astragalusScientific

  AS-IV and astragalus root extracts demonstrate well-characterized hepatoprotective activity in preclinical models for liver injury, fibrosis, NAFLD, and hepatitis. NIH LiverTox confirms hepatoprotective activity in animal models and documented clinical use in TCM for hepatitis. Mechanistic pathways include Nrf2/HO-1, NF-κB, and TGF-β/Smad signaling.

• atractylodesScientific

  Atractylodes macrocephala polysaccharides show documented hepatoprotective activity in drug-induced and diet-induced liver injury models, reducing liver enzymes, oxidative stress, and inflammatory pathways. The herb is traditionally associated with the liver meridian in TCM.

• baikal skullcapScientific

  Baicalin from S. baicalensis is among the most studied hepatoprotective natural compounds, demonstrating protection against viral hepatitis, NAFLD/NASH, xenobiotic liver injury, cholestatic liver injury, and hepatocellular carcinoma through multiple mechanisms. Clinical use for hepatitis in China is well documented.

• bambooScientific

  Bamboo stem and leaf extracts protect the liver from oxidative damage, lipotoxicity, and alcohol-induced injury in animal models. Bamboo polyphenols activate the Nrf2/HO-1 hepatoprotective pathway. BEX in obese-diabetic mice significantly lowered hepatic fat content, improved glucose tolerance, and reduced hepatic inflammatory cytokines.

• banabaScientific

  Banaba leaf extract demonstrates hepatoprotective activity in animal and zebrafish models, reducing hepatic lipid accumulation, preventing fatty liver changes, lowering liver enzyme markers, and reducing inflammatory infiltration. Corosolic acid in obese mice reduced hepatic lipids by up to 65%. The Philippine herbal medicine system lists hepatoprotective effects among banaba's documented uses.

• barberryScientific

  Multiple clinical trials show barberry/berberine protects the liver, reducing ALT and AST enzymes in NASH patients, and a 500 mg berberine three times daily for 16 weeks significantly reduced liver fat in 184 patients. Barberry also stimulates bile secretion and is a traditional liver tonic.

• barleyScientific

  Barley sprout extract has demonstrated hepatoprotective effects in a 12-week RCT in habitual drinkers with fatty liver, reducing oxidative stress and supporting glutathione antioxidant defense. Barley β-glucan also reduces hepatic cholesterol load by interrupting bile acid recirculation.

• basilScientific

  A PMC-published RCT in rats (2021) showed rosmarinic acid-rich extract from O. basilicum significantly reduced hepatic enzyme markers (AST, ALT, ALP) in CCl4-intoxicated animals. A 2026 Metabolomics study found basil-enriched oil improved liver lipid accumulation and oxidative stress. Oleanolic acid in basil has documented hepatoprotective properties.

• bayberryScientific

  A completed randomized, double-blind, placebo-controlled crossover trial (n=44) found bayberry juice improved antioxidant status and reduced inflammatory and apoptotic markers in NAFLD patients. Traditional use for jaundice and liver toning is also documented. Drugs.com confirms 'some protective effects on the liver were seen in 1 small study.'

• bee pollenScientific

  Bee pollen's polyphenols protect hepatocytes from chemical-induced oxidative damage in multiple animal models, reducing AST/ALT elevations, hepatic steatosis, and apoptosis. In vitro studies on human liver cell lines confirm antisteatosis and antioxidant hepatoprotection. Traditional apitherapy records include liver tonic use.

• beetScientific

  Betaine, concentrated in beetroot, protects the liver via BHMT-mediated remethylation of homocysteine, maintenance of SAMe levels, and reduction of hepatic lipid accumulation and oxidative stress. Preclinical studies demonstrate hepatoprotective effects; human evidence is limited but mechanistically compelling.

• belleric myrobalanScientific

  Multiple preclinical studies confirm T. bellirica hepatoprotective activity against drug-induced liver injury (diclofenac, aceclofenac, CCl4 models), reducing liver enzyme markers and fibrosis, with ellagic acid showing effects comparable to silymarin. A 2022 study demonstrated protection against NAFLD in mice. Traditional use for liver protection spans Ayurveda, Tibetan, and Chinese medicine.

• berberineScientific

  Berberine has well-documented clinical evidence supporting its use in non-alcoholic fatty liver disease (NAFLD/MAFLD). Multiple randomized controlled trials and meta-analyses demonstrate that berberine reduces hepatic fat content, improves liver enzyme profiles, and corrects associated dyslipidemia. The primary mechanism involves AMPK activation, which suppresses hepatic triglyceride synthesis and promotes lipid oxidation. Evidence is promising but current trials are generally small and more high-quality RCTs are needed.

• beta and delta tocopherolsScientific

  Delta-tocopherol (and related delta-tocotrienol) has been specifically studied for reducing hepatic steatosis and oxidative stress in non-alcoholic fatty liver disease. A 48-week randomized double-blind trial showed delta-tocotrienol (a structural analog) produced equivalent improvements in hepatic steatosis, insulin resistance, and oxidative stress as alpha-tocopherol. Delta-tocopherol reduces oxidative stress and fat accumulation in liver cells per ongoing research.

• betaineScientific

  Betaine is a methyl donor that supports liver health by participating in the methionine cycle, reducing homocysteine, and maintaining hepatic S-adenosylmethionine (SAM) levels. Multiple human and animal studies have examined its role in nonalcoholic fatty liver disease (NAFLD/NASH) and alcoholic liver disease, with mixed but generally supportive results. Clinical evidence includes randomized controlled trials, though effect sizes in humans are modest and some trials have failed to show significant benefit beyond slowing disease progression.

• betelScientific

  P. betle and especially red betel (Piper crocatum) exhibit hepatoprotective effects, reducing liver enzyme markers, TNF-α, ROS, and necrotic cell death in cell and rodent models of chemical liver injury. Antioxidant and anti-inflammatory mechanisms are central.

• bifidobacterium bifidumScientific

  B. bifidum ameliorates non-alcoholic/metabolic-associated fatty liver disease (NAFLD/MAFLD) in animal models by reprogramming hepatic mitochondrial lipid metabolism via the PPAR-α/PGC-1α/CPT1A axis, reducing steatosis and improving hepatocyte morphology. It also modulates gut microbiota and FXR expression to reduce liver lipid deposition and insulin resistance. Broader Bifidobacterium genus human data support reductions in serum aminotransferases and liver fat.

• bile saltScientific

  The liver synthesizes all primary bile salts from cholesterol, constituting the primary route of cholesterol catabolism. Bile salt signaling via FXR controls hepatic lipogenesis, gluconeogenesis, and cholesterol homeostasis. Dysregulation of bile salt transport and synthesis is implicated in cholestatic liver disease, NAFLD/MASLD, and primary biliary cholangitis, with FXR agonists (e.g., obeticholic acid) now FDA-approved for primary biliary cholangitis.

• black cuminScientific

  A systematic review of 4 RCTs in NAFLD found N. sativa significantly reduced hepatic steatosis grade and liver enzymes in 3 of 4 trials. The 2025 meta-analysis of 82 RCTs confirmed significant improvements in ALT, AST, and ALP. Thymoquinone is hepatoprotective via NF-κB inhibition, CYP2E1 modulation, and reduction of hepatocyte lipid peroxidation.

• black pepperScientific

  Piperine has demonstrated hepatoprotective activity by reducing liver enzyme leakage and oxidative stress in animal hepatotoxicity models. A large 2025 RCT in 170 NAFLD patients found piperine supplementation significantly improved hepatic lipid and metabolic markers. A pilot human study reported piperine-combination benefit in hepatocellular carcinoma patients.

• black teaScientific

  Black tea polyphenols demonstrate hepatoprotective antioxidant effects in animal models, reducing oxidative damage markers in liver tissue. Evidence includes protection against ethanol-induced lipid peroxidation in liver and preclinical support for reduced non-alcoholic fatty liver disease progression via gut microbiota modulation.

• blackboard treeScientific

  Hepatoprotective activity of A. scholaris bark extracts has been demonstrated in paracetamol- and ethanol-induced liver damage models in rats, with significant reductions in AST, ALT, and ALP. Indole alkaloids also attenuated NAFLD-associated liver injury markers in a high-fat-diet mouse model.

• boxthorneScientific

  LBPs are hepatoprotective across ethanol, CCl4, NAFLD, cadmium, and heavy metal liver injury models, modulating PPAR-α, NLRP3/Caspase-1, apoptosis, and oxidative stress pathways. TCM specifies boxthorn as a liver-nourishing herb. A 2025 human clinical review identifies NAFLD as among the conditions for which human studies highlight L. barbarum's therapeutic potential.

• broccoliScientific

  The liver is a primary site of sulforaphane action. Human RCTs show broccoli sprout extract significantly improves liver function markers (ALT, AST, GGT) in NAFLD patients. Sulforaphane induces hepatic phase II detoxification enzymes via Nrf2, reduces hepatic oxidative stress, and improves fatty liver disease in clinical trials.

• broomrapeScientific

  Orobanche foetida and O. crenata have demonstrated hepatoprotective effects in rodent models, including protection against CCl4-induced liver injury via antioxidant enzyme boosting and anti-inflammatory cytokine downregulation. Traditional use for liver obstruction and jaundice is also documented across Western and TCM traditions.

• brown rice proteinScientific

  Rice protein peptides have been shown to exhibit hepatoprotective effects by reducing hepatic fat accumulation, increasing antioxidant enzyme activity, and decreasing pro-inflammatory cytokines (Food & Function, 2025 mouse model). Brown rice and germinated brown rice also protect against non-alcoholic fatty liver disease in animal models by reducing hepatic lipid deposition and modulating lipid metabolism genes. Rice protein reduces hepatic triglyceride output by suppressing CD36 and MTP expression (PMC, 2024).

• brussel sproutsScientific

  Brussels sprouts-derived I3C and DIM induce hepatic Phase I (CYP1A1, CYP1A2) and Phase II (glutathione S-transferases, Nrf2-target enzymes) detoxification pathways. Human studies confirm increased plasma GST-alpha after Brussels sprouts consumption. The liver is the primary site of glucosinolate metabolite bioactivation.

• bupleurumScientific

  Bupleurum has deep roots in Traditional Chinese Medicine (TCM) as a primary herb for liver conditions, and this is supported by a substantial body of preclinical (in vitro and animal) research demonstrating hepatoprotective, anti-inflammatory, and anti-fibrotic effects. Human clinical evidence exists, principally through trials of the Bupleurum-containing formula Sho-saiko-to (Xiao Chai Hu Tang), which showed reductions in liver enzyme levels, hepatitis symptoms, and hepatocellular carcinoma incidence in cirrhotic patients. However, rigorous standalone human trials of isolated Bupleurum are lacking, and the bioactive saikosaponins carry a dose-dependent hepatotoxicity risk.

• bupleurum falcatumScientific

  Bupleurum falcatum has documented traditional use in Chinese medicine for liver complaints and is backed by preclinical (animal/in vitro) scientific evidence for hepatoprotection via its key actives, the saikosaponins. Human clinical evidence exists, but only in the context of multi-herb formulas (notably Sho-saiko-to), not for the isolated herb. Evidence for the mono-herb in humans remains lacking, qualifying the scientific designation as preliminary and formula-level rather than herb-specific.

• burdockScientific

  Burdock root has demonstrated hepatoprotective effects in multiple preclinical studies, protecting against alcohol, carbon tetrachloride, acetaminophen, cadmium, and lead-induced liver damage. Lin et al. (J Biomed Sci, 2002) is cited in the EMA reference list. A 2023 lab study found burdock reduced hepatic fat accumulation. Preclinical evidence is strong; human clinical trials are limited.

• butyric acidScientific

  Butyrate shows hepatoprotective effects in NAFLD/MAFLD via the gut-liver axis, reducing hepatic lipid accumulation, oxidative stress, and intestinal permeability that drives endotoxemia. A human RCT in liver steatosis and metabolic syndrome has been conducted.

• cabbageScientific

  Sulforaphane from cabbage activates hepatic Nrf2 signaling, upregulating Phase II detoxification enzymes and protecting against oxidative liver damage. Cabbage juice attenuated liver enzyme elevations (ALT, AST, ALP) in a rodent liver-damage model. I3C/DIM from cabbage also induces hepatic CYP1A enzymes, modulating hormone and xenobiotic metabolism.

• caesalpinia cristaScientific

  C. crista leaf and seed extracts have demonstrated hepatoprotective activity against CCl4 and iron-overload-induced liver toxicity in animal models. PMC-indexed studies confirm protection via antioxidant and iron-chelating mechanisms, with normalization of liver enzymes and reduction of fibrosis.

• campesterolScientific

  The liver is the secondary site of campesterol's metabolic activity: reduced intestinal cholesterol absorption triggers compensatory hepatic LDL receptor upregulation and cholesterol synthesis. ABCG5/8 transporters are expressed in both the intestine and liver, regulating biliary secretion of campesterol. Campesterol may also modulate hepatic cholesterol-transporting protein synthesis and lipoprotein assembly.

• camu camuScientific

  The 2024 Université Laval RCT (Cell Reports Medicine; n=30; 12 weeks; 1.5 g/day) showed camu camu extract decreased liver fat by 7.43% (MRI-measured) versus an 8.42% increase on placebo — a 15.85% differential — and also reduced AST and ALT liver injury markers. Prior mouse studies established CC's hepatoprotective and anti-steatotic effects in diet-induced obesity.

• capsanthinScientific

  Capsanthin accumulates in the liver and exerts hepatoprotective effects in NAFLD models by reducing hepatic steatosis, normalizing ALT/AST, and regulating fatty acid metabolism gene expression. It also modulates HDL-C metabolism through hepatic LCAT and ApoA5 upregulation.

• cardamomScientific

  Green cardamom's hepatoprotective effects have been studied in human NAFLD patients (RCT, n=87) and in preclinical models of toxic liver injury. Cardamom raises Sirtuin-1, reduces liver enzyme elevation, and suppresses hepatic oxidative stress and inflammation via the Nrf2/HO-1/NQO-1 pathway.

• carrotScientific

  Carrot extracts have demonstrated hepatoprotective effects in multiple animal models, reducing liver enzyme elevations and histological damage following chemical injury. Black carrot showed hepatoprotection in a rat sepsis model. Retinoic acid derived from carrot beta-carotene modulates hepatic immune responses. Animal data are extensive; direct human clinical evidence is limited.

• caryophylleneScientific

  BCP protects the liver from alcohol-induced steatohepatitis, NAFLD, fibrosis, and hepatotoxin-induced injury via CB2 receptor activation, PPAR-α/γ engagement, antioxidant replenishment, and suppression of hepatic stellate cell activation.

• cascara sagradaScientific

  Cascara sagrada has a clinically documented relationship with the liver primarily through hepatotoxicity. Case reports and case series have linked it to cholestatic hepatitis, portal hypertension, and acute liver failure. NIH LiverTox classifies it as a hepatotoxin at high doses or with prolonged use. Separately, emodin (a constituent) has shown hepatoprotective effects in animal studies, but human evidence for liver benefit is absent.

• cassia barkScientific

  C. cassia extract restored hepatic enzyme markers (AST, ALT, ALP) in diabetic animal models, and a systematic review of cinnamon supplementation effects on liver enzymes in adults was identified. However, cassia bark's coumarin content is also a known hepatotoxicity risk at high doses.

• catalaseScientific

  The liver contains among the highest concentrations of catalase of any organ in the body, reflecting its central role in hepatic H₂O₂ metabolism and detoxification. Liver catalase is critical for neutralizing H₂O₂ generated by fatty acid β-oxidation in peroxisomes. Catalase deficiency in acatalasemia leads to hepatic lipid accumulation and metabolic dysfunction.

• catechinsScientific

  Catechins exert hepatoprotective effects by reducing liver triglyceride accumulation, attenuating oxidative and inflammatory liver damage, and modulating lipid synthesis gene expression. A systematic review concluded green tea catechins are a potentially useful treatment for NAFLD. High-dose catechin extracts can paradoxically cause hepatotoxicity.

• catjang cowpeaScientific

  Cowpea protein has been shown to reduce liver steatosis in hamster models. Fermented and unfermented cowpea also positively affected liver weight in animal studies. The lipid-lowering and antioxidant properties of cowpea have direct hepatoprotective implications.

• cauliflowerScientific

  Sulforaphane from cauliflower is a potent hepatoprotective compound that activates Nrf2 in liver cells, induces phase II detoxification enzymes, reduces hepatic oxidative stress and inflammation, and has been studied in models of alcoholic and drug-induced liver injury. Choline from cauliflower prevents hepatic fat accumulation.

• celeryScientific

  A clinical RCT (n=51, 4 weeks, 1.34 g/day) found celery seed extract significantly reduced liver enzymes SGPT and SGOT. Animal studies show protection against acetaminophen- and carbon tetrachloride-induced liver injury. Celery also activates the Nrf2 antioxidant signaling pathway in a mouse model of hepatorenal injury.

• chaff flowerScientific

  Hepatoprotective activity of A. aspera is consistently demonstrated across multiple preclinical studies covering oxidative liver damage, high-cholesterol hepatotoxicity, and lipid peroxidation reduction. It is one of the most replicated pharmacological findings for this plant.

• chen piScientific

  Chen Pi flavonoids (hesperidin, naringin, nobiletin) protect hepatic cells from oxidative and inflammatory injury via Nrf2 pathway activation and PI3K-Akt modulation. Systems pharmacology analyses identify multiple hepatoprotective targets; CRP is used clinically in China for liver-related conditions.

• chickweedScientific

  A published rodent study demonstrated hepatoprotective activity of S. media polysaccharide fraction in CCl4-induced hepatitis, reducing liver enzyme levels and hepatic damage. An in vitro study also showed anti-HBV activity in liver cells. Traditional use for liver heat-clearing exists.

• chicoryScientific

  Chicory (Cichorium intybus) has documented clinical and preclinical evidence supporting hepatoprotective effects, particularly in non-alcoholic fatty liver disease (NAFLD). A 2023 systematic review and meta-analysis of five randomized clinical trials (n=197 NAFLD patients) found that chicory supplementation significantly reduced the liver enzymes AST and ALT. Preclinical work attributes these effects to antioxidant, anti-inflammatory, and nuclear-receptor-modulating mechanisms involving bioactives such as chicoric acid, inulin, and sesquiterpene lactones.

• chinese salvia rootScientific

  The liver is explicitly one of Danshen's primary organ targets, entering the 'liver meridian' in TCM. Modern evidence confirms hepatoprotective effects across NAFLD, alcoholic liver disease, hepatic fibrosis, and viral hepatitis. Eight RCTs in NAFLD patients showed significant transaminase reduction.

• chlorellaScientific

  Multiple randomized controlled trials (RCTs) and a meta-analysis of 7 RCTs have examined Chlorella vulgaris supplementation and liver function, primarily in non-alcoholic fatty liver disease (NAFLD). The meta-analysis found a significant reduction in serum AST levels (WMD −9.15 U/L), with stronger effects in NAFLD subgroups. A separate clinical study in chronic hepatitis C patients also reported significant ALT reductions. Evidence is promising but not yet conclusive, with heterogeneity across trials noted.

• chlorophyllScientific

  Chlorophyllin protects the liver from aflatoxin-induced genotoxic damage in a landmark human RCT (55% reduction in DNA adduct biomarkers; Johns Hopkins/Qidong, PNAS 2001). Animal studies further show chlorophyllin ameliorates NAFLD, hepatic fibrosis, and liver inflammation by modulating gut microbiota and suppressing hepatic NF-κB signaling. The liver is the primary organ at risk from AFB1 and the primary target of chlorophyllin's chemoprotective action.

• chlorophyllinScientific

  The liver is the primary target organ in the most robustly evidenced human trial of chlorophyllin. The Kensler/Egner PNAS 2001 RCT (n=180) demonstrated a 55% reduction in hepatic DNA damage biomarkers (aflatoxin-DNA adducts) with chlorophyllin 100 mg three times daily for 4 months. A 2018 mouse study further demonstrated that oral chlorophyllin reduced hepatic fibrosis and liver inflammation via gut-liver axis modulation.

• chokeberryScientific

  Animal studies consistently demonstrate chokeberry's hepatoprotective effects: reducing liver lipid accumulation, lowering serum transaminases, improving liver antioxidant capacity, and protecting against toxin-induced acute liver injury. Mechanisms include Nrf2 pathway activation and PPARγ2 downregulation. Human clinical liver-specific evidence is lacking.

• cholineScientific

  Choline is essential for hepatic phosphatidylcholine synthesis, which is required for VLDL assembly and triglyceride export from the liver. Deficiency consistently causes hepatic steatosis and elevated liver enzymes in human depletion studies. Adequate choline intake is linked to reduced risk and severity of nonalcoholic fatty liver disease (NAFLD), and supplementation has reversed NAFLD in TPN-dependent patients in clinical trials. Both the NIH Office of Dietary Supplements and EFSA recognize the cause-and-effect relationship between choline intake and normal liver function.

• chrysanthemumScientific

  Chrysanthemum demonstrates hepatoprotective, lipid-normalizing, and antioxidative effects in multiple preclinical models. The herb is pharmacopoeially listed in TCM for liver-related indications. A 2025 Scientific Reports study and earlier PMC animal studies show protection against chemically induced liver injury and fatty liver via Nrf2 pathway activation.

• chrysinScientific

  Chrysin is one of the best-characterized hepatoprotective flavonoids in preclinical research, with documented protection against chemical hepatotoxins (CCl4, d-galactosamine, paracetamol, doxorubicin), alcohol-induced injury, NAFLD, hepatic fibrosis, and encephalopathy. Mechanisms include antioxidant enzyme restoration, lipid peroxidation suppression, and anti-inflammatory cytokine reduction.

• cinnamonScientific

  Cinnamon modulates hepatic glucose metabolism via pyruvate kinase and PEPCK enzymes, inhibits hepatic HMG-CoA reductase, and in clinical studies reduces transaminase (ALT/AST) and lipid peroxidase activities. A 2025 GRADE meta-analysis of 49 RCTs included liver enzymes (ALT, AST, ALP) among its assessed outcomes.

• citrus pectinScientific

  Citrus pectin indirectly benefits the liver by reducing hepatic cholesterol load through bile-acid sequestration and by promoting liver bile-acid synthesis via gut-microbiota-derived indole-3-lactic acid. Animal models show pectin alleviates hepatic lipid accumulation (MAFLD/NAFLD) through gut–liver axis mechanisms. Preclinical rat studies also showed citrus peel pectin restored liver function markers.

• citrus sinensisScientific

  Naringenin and hesperidin from C. sinensis demonstrate hepatoprotective effects in preclinical models, reducing liver enzymes and oxidative stress. A clinical RCT found daily orange consumption reduced hepatic steatosis prevalence in MASLD patients. Hesperidin promotes hepatic fatty acid β-oxidation via SIRT1/PGC1α.

• cleaversScientific

  A 2022 rodent study demonstrated G. aparine significantly reduced APAP-induced liver damage, lowering ALT, AST, and bilirubin. A second rodent study found hepatoprotective effects in a CCl₄ model. Traditional use for jaundice corroborates this. No human trials exist.

• cloveScientific

  Eugenol-rich clove fractions have demonstrated hepatoprotective effects in multiple preclinical models, reversing biochemical and histopathological signs of liver cirrhosis, fatty liver, and toxic hepatopathy. A human pilot study noted liver function and redox benefits.

• coconutScientific

  MCTs in coconut oil are primarily metabolized in the liver, where they undergo rapid beta-oxidation and ketogenesis. Animal models show coconut oil diet reduces hepatic fat accumulation and liver inflammation gene expression versus lard. Human liver-specific clinical data are limited; MCT-based nutrition is used in clinical hepatology for fat malabsorption.

• coffee fruitScientific

  Coffee fruit's chlorogenic acid and colonic metabolites of CGAs have demonstrated hepatoprotective effects. Coffee pulp phenolic compounds preserve glutathione, SOD, and catalase in hepatic HepG2 cells under oxidative stress. CGA reduces hepatic triglyceride synthesis and glucose-6-phosphatase activity. Colonic CGA metabolites protect hepatic cells from TNF-α-induced inflammation and oxidative stress.

• coixScientific

  Coix seed extracts reduce hepatic fat accumulation, liver oxidative stress, and liver enzyme elevations in multiple NAFLD and hyperlipidemia animal models. The mechanisms include AMPK activation, PPAR signaling, inhibition of lipogenesis genes, and liver cholesterol synthesis suppression.

• collardScientific

  Collard greens' glucosinolates activate hepatic phase II detoxification enzymes (glutathione S-transferases), facilitating carcinogen and xenobiotic conjugation and elimination. Collards boost intracellular glutathione — the liver's primary antioxidant and detoxification molecule. A human RCT using cruciferous vegetables demonstrated significantly increased urinary excretion of benzene carcinogens, directly evidencing hepatic phase II induction.

• commiphoraScientific

  Commiphora myrrh extract demonstrates hepatoprotective activity in animal models of alcohol-induced hepatotoxicity, reducing oxidative stress, inflammatory infiltrate, necrosis, and fibrosis. Multiple Commiphora species show protective effects against lipid peroxidation-related hepatic damage.

• copperScientific

  The liver is the central organ regulating copper homeostasis. It synthesizes and secretes ceruloplasmin, excretes excess copper into bile, and stores copper in hepatocytes. Copper dysregulation (Wilson's disease excess; acquired deficiency post-bariatric surgery) directly causes hepatic pathology. Copper is essential for hepatic antioxidant defense (Cu/Zn-SOD) and lipid metabolism.

• coptis chinensisScientific

  Coptis chinensis demonstrates hepatoprotective effects in multiple animal models, reducing ALT/AST elevations, combating hepatic steatosis, and modulating lipid metabolism via AMPK/SREBP-1c and PPARα/LXRα pathways. TCM uses the herb to 'clear heat in the liver' and TCM formulas are used for hepatitis.

• CoQ10 (coenzyme Q10)Scientific

  CoQ10 has human clinical evidence supporting its role in liver health, primarily through its antioxidant and mitochondrial bioenergetics properties. Multiple RCTs and meta-analyses demonstrate that CoQ10 supplementation significantly reduces liver enzymes (ALT, AST, GGT) and reduces hepatic steatosis in conditions such as NAFLD/MASLD. Evidence is promising but individual study sizes remain modest and results are not uniformly consistent across all outcomes.

• cordycepsScientific

  Cordyceps militaris exhibits hepatoprotective effects in animal models of NAFLD, NASH, and high-fat diet–induced liver damage, reducing ALT, AST, hepatic lipid accumulation, triglycerides, inflammation, and fibrosis. Antioxidant mechanisms—including increased hepatic GSH and reduced lipid peroxidation—contribute to liver protection. Human safety data confirm no hepatotoxicity; therapeutic human trials are absent.

• cornsilkScientific

  Multiple preclinical studies show corn silk extract protects the liver against chemical-induced toxicity, reduces liver enzyme levels (AST, ALT), improves liver histopathology, and modulates liver lipid metabolism. A 2026 Scientific Reports study demonstrated corn silk ameliorates fatty liver disease in high-fat diet mice via gut microbiota modulation.

• cryptoxanthinScientific

  Epidemiological studies show serum BCX is inversely associated with NAFLD risk and severity. Mechanistic animal studies demonstrate BCX reduces hepatic steatosis, inflammation (NF-κB, TNF-α), and insulin resistance while activating PPAR-α and shifting M1/M2 macrophage balance in the liver.

• cucumberScientific

  Multiple animal studies demonstrate hepatoprotective effects of cucumber extract against chemical liver injury (cumene hydroperoxide, CCl4) and diabetes-induced hepatic damage, with normalisation of ALT/AST and restoration of hepatic histopathology. Aqueous cucumber fruit extract acts as a hepatoprotective antioxidant in validated assays.

• cuminScientific

  Cumin significantly stimulates hepatic bile secretion (bile volume +25%, bile acid output up to +70% over control in animal studies). One RCT evaluated cumin in NASH patients. Its antioxidants reduce hepatic oxidative stress and oxidized LDL. Traditional use for jaundice and liver complaints is well documented.

• curcuminScientific

  Curcumin has been investigated in multiple randomized controlled trials and meta-analyses for liver support, particularly in non-alcoholic fatty liver disease (NAFLD). Clinical evidence shows significant reductions in the liver enzymes ALT and AST following curcumin supplementation. Mechanistically, curcumin acts via antioxidant, anti-inflammatory, and anti-fibrotic pathways. Evidence quality is rated low-to-moderate, and further high-quality trials are needed to confirm efficacy and optimal dosing.

• d-alpha tocopherolScientific

  D-alpha tocopherol is the most evidence-supported antioxidant supplement for liver health, with multiple RCTs demonstrating improvements in hepatic steatosis, inflammation, and liver enzymes in NAFLD/NASH. Its hepatoprotective role is confirmed by the NIH LiverTox database and a 2024 PMC systematic review.

• daidzinScientific

  Daidzein and daidzin demonstrate hepatoprotective effects in animal models, reducing liver injury markers, oxidative stress, and inflammation. In diabetic animals, daidzin modulates hepatic gluconeogenic and lipogenic enzyme activities. A rat hepatocellular carcinoma model showed daidzein reduced all HCC markers.

• damianaScientific

  Damiana's LXR agonism (2.7-fold in a 2025 in vitro study) is relevant to hepatic lipid metabolism, and NRF2 activation supports hepatic antioxidant defense. Arbutin's immunomodulatory properties have anti-inflammatory relevance. Evidence is limited to in vitro and animal research; traditional use for liver conditions is not prominently documented.

• danshenScientific

  Danshen (Salvia miltiorrhiza) has documented hepatoprotective effects supported by both traditional use and a growing body of clinical and preclinical evidence. Key active compounds—tanshinones (especially Tanshinone IIA) and salvianolic acids (especially Salvianolic Acid B)—demonstrate anti-fibrotic, antioxidant, and anti-inflammatory actions in the liver. Human-level evidence includes a meta-analysis of 11 RCTs in liver cirrhosis patients and a separate meta-analysis of 8 RCTs in NAFLD patients, though trial quality remains limited and larger confirmatory studies are still needed.

• delta-tocopherolScientific

  Delta-tocopherol and its tocotrienol analogue have been clinically studied in NAFLD, demonstrating significant reductions in hepatic steatosis, oxidative stress markers (malondialdehyde), insulin resistance, and inflammation. A 48-week double-blind RCT (n=100) showed both δ-tocotrienol and α-tocopherol equally improved fatty liver index and liver-to-spleen ratio, with δ-tocotrienol superior for inflammation and apoptosis reduction. Tocotrienol forms penetrate fatty liver tissue more efficiently than tocopherols.

• dihydromyricetinScientific

  Dihydromyricetin (DHM) is a flavonoid with well-documented hepatoprotective activity supported by both preclinical research and at least one human randomized controlled trial. It has been studied across multiple liver conditions including NAFLD, alcoholic liver disease, drug-induced hepatotoxicity, and fibrosis. Key mechanisms involve anti-inflammatory (NF-κB suppression), antioxidant, and sirtuin-dependent (SIRT3/AMPK) pathways. Human clinical evidence exists but remains limited in scale, and further large trials are ongoing.

• DIM (diindolylmethane)Scientific

  DIM is a well-documented inducer of hepatic Phase I (CYP1A1, CYP1A2, CYP3A4) and Phase II detoxification enzymes, directly acting on liver metabolism of estrogens and xenobiotics. A PMC study demonstrated DIM protected against CCl4-induced chronic liver injury in mice via Nrf2 pathway activation. In multiple human clinical trials, liver function tests (LFTs) remained normal with DIM supplementation.

• dioscoreaScientific

  Diosgenin and dioscin from Dioscorea spp. demonstrate hepatoprotective effects across multiple animal and cell studies, preventing liver injury, fibrosis, fatty liver, and steatohepatitis. A 2023 PMC literature review comprehensively catalogues these mechanisms. Human evidence is absent.

• dodderScientific

  Cuscuta spp. demonstrate significant hepatoprotective effects in multiple preclinical models. Both aqueous and methanolic C. arvensis extracts significantly reduced liver damage markers (ALT, AST, ALP, bilirubin) in acetaminophen-induced hepatotoxicity in rats. C. chinensis nanoparticle formulations also show hepatoprotective effects. Antioxidant mechanisms protecting mitochondrial function are the primary proposed pathway.

• dogwoodScientific

  Cornus officinalis is a principal TCM liver-tonifying herb with documented preclinical hepatoprotective effects. Animal studies show protection against liver injury from toxins, high-fat diets, and diabetic damage, mediated through Nrf2 pathway activation and antioxidant mechanisms. Extracts have also shown anti-hepatocellular carcinoma activity in vitro.

• dong quaiScientific

  A. sinensis polysaccharides have demonstrated hepatoprotective activity in preclinical models, including protection against acetaminophen-induced hepatic damage. The herb is used in TCM for chronic hepatitis and cirrhosis. An MDPI 2026 review confirmed hepatoprotection as among the documented activities of Dong Quai's major bioactive components.

• EGCG (epigallocatechin gallate)Scientific

  EGCG (epigallocatechin gallate), the predominant bioactive catechin in green tea, has clinical and extensive preclinical evidence supporting hepatoprotective effects, particularly in non-alcoholic fatty liver disease (NAFLD). It modulates key signaling pathways involved in hepatic oxidative stress, inflammation, lipid accumulation, and fibrosis. Clinical studies are promising but limited in number and scale, and paradoxically, high doses of EGCG have been associated with dose-dependent hepatotoxicity.

• eicosapentaenoic acidScientific

  EPA reduces hepatic steatosis, inhibits VLDL synthesis, and reduces liver inflammation, with mechanistic evidence in non-alcoholic fatty liver disease (NAFLD). EPA reversed obesity-induced hepatic steatosis in animal models and modulates hepatic miRNA and gene expression pathways linked to lipid metabolism.

• eicosenoic acidScientific

  Gondoic acid (cis-11-eicosenoic acid) has been directly studied in Kupffer cells — the liver's resident macrophages — where it inhibited pro-inflammatory factor expression, reduced ROS, and blocked PKCθ/ERK/STAT3 signaling in LPS-stimulated cells. LCMUFA-rich marine oils containing eicosenoic acid have also attenuated hepatic steatosis in animal models. Evidence is preclinical (in vitro and animal), with no human liver-specific trials on isolated eicosenoic acid.

• eleutheroScientific

  Eleuthero has documented hepatoprotective activity in animal models of chemically-induced liver injury. Active polysaccharide and phenolic constituents reduce liver damage markers (ALT, AST), increase antioxidant enzymes, and suppress NF-κB-mediated hepatic inflammation. Traditional use includes treatment of hepatitis.

• enicostemma littoraleScientific

  Hepatoprotective and hepatomodulatory activity is among the best-documented preclinical effects of E. littorale, with evidence in paracetamol-, D-galactosamine-, ethanol-, and CCl4-induced liver injury models in rats. Swertiamarin is identified as the key hepatoprotective compound. Liver enzyme normalization, antioxidant restoration, and lipid reduction in hepatic tissue are consistently demonstrated.

• EPA (eicosapentaenoic acid)Scientific

  EPA and DHA supplementation has been evaluated extensively in non-alcoholic fatty liver disease (NAFLD), with the majority of human studies reporting reductions in liver fat, liver enzymes, or inflammatory markers. EPA-specific mechanistic studies show it reduces hepatic steatosis by modifying lipid metabolism gene expression and reducing hepatic inflammation via miRNA-mediated pathways.

• eucommiaScientific

  Eucommia leaf and bark extracts show hepatoprotective effects in multiple chemical-induced liver injury models (CCl4, APAP), reducing liver enzymes, improving glutathione status, and reducing histopathological injury. Network pharmacology analyses support anti-inflammatory, antioxidative, and cytoprotective mechanisms in hepatic ischemia-reperfusion injury.

• fennelScientific

  Fennel essential oil and seed extracts demonstrate hepatoprotective activity in multiple animal models of chemically induced liver damage, reducing AST, ALT, ALP, and bilirubin levels. Traditional pharmacopeias list fennel as hepatoprotective. Human liver studies are absent.

• fenugreekScientific

  Fenugreek exerts hepatoprotective effects by reducing oxidative stress, modulating bile composition, influencing hepatic metabolic pathways, and protecting against liver injury. The NIH LiverTox database confirms no clinically apparent liver injury, with robust preclinical hepatoprotective data. Emerging clinical signals from an NAFLD pilot RCT exist.

• ferula assafoetidaScientific

  Asafoetida exhibits hepatoprotective activity documented in multiple animal models of chemical-induced hepatotoxicity. A 2025 PMC review specifically examines its protection of the liver against formaldehyde-induced damage. The herb stimulates bile acid production and normalizes liver enzyme markers.

• ferulic acidScientific

  Ferulic acid is hepatoprotective across multiple models of liver injury: it reduces AST, ALT, and ADH activity in drug-induced hepatotoxicity, inhibits liver fibrosis and hepatocyte apoptosis, and has shown benefits in clinical trials for liver cirrhosis. FA modulates hepatic lipid metabolism (SREBP1c, CPT1a, PPARα) and activates Nrf2-mediated cytoprotective pathways in liver cells.

• fisetinScientific

  Fisetin exerts hepatoprotective effects through NF-κB, Nrf2, AMPK, and SIRT1 pathway modulation, reducing hepatic inflammation, oxidative stress, steatosis, and fibrosis. A 2025 PMC review systematically characterized its potential in IFALD.

• fish oilScientific

  Fish oil omega-3s have demonstrated hepatoprotective effects relevant to non-alcoholic fatty liver disease (NAFLD). EPA and DHA improve hepatic lipid metabolism, reduce hepatic triglyceride accumulation, and alleviate hepatic inflammation via multiple pathways. Clinical and animal studies show fish oil protects the liver against Western diet-induced NAFLD.

• flaxseedScientific

  Flaxseed's ALA omega-3 and SDG lignans support liver health by reducing fat accumulation, oxidative stress, and inflammation. An animal study demonstrated flaxseed oil prevented hepatic encephalopathy. A broader cardiovascular review linked flaxseed components to reduced risk of metabolic dysfunction-associated steatotic liver disease (MASLD).

• flowering quinceScientific

  C. speciosa is listed in TCM for hepatitis treatment, and pharmacological studies confirm hepatoprotective activity as a key property. The fruit has been applied clinically in China for viral hepatitis, and multiple reviews cite hepatoprotective activity as experimentally confirmed.

• forsythiaScientific

  Hepatoprotective properties of Forsythia suspensa are supported by multiple preclinical studies, with forsythoside A protecting against oxidative liver damage via MDA clearance. New iridoid glycosides from the fruit have confirmed hepatoprotective activities. Forsythia root has traditional use for jaundice. Fulminant hepatitis prevention was demonstrated in a mouse model.

• fu lingScientific

  Poria cocos polysaccharides demonstrate hepatoprotective effects in alcohol-induced liver injury, LPS/D-galactosamine-induced acute liver failure, and MAFLD models in rodents. Mechanisms include NF-κB/PI3K-AKT pathway modulation, antioxidant enzyme restoration, lipid metabolism regulation via FXR/PPARα-SREBPs, and reverse cholesterol transport.

• fulvic acidScientific

  Fulvic acid chelates toxins and heavy metals and supports hepatic detoxification pathways including glutathione and SOD activity. Animal models show fulvic acid protects liver function under metabolic stress. Traditional Ayurvedic and veterinary use of humic acid for liver protection is documented.

• ganodermaScientific

  Ganoderma lucidum has the strongest human clinical evidence for hepatoprotective effects among body systems. A double-blind crossover RCT in healthy volunteers showed significant improvement in liver enzymes and antioxidant capacity, with reversal of fatty liver on ultrasound. Multiple hepatoprotective mechanisms are confirmed.

• garbanzo beanScientific

  Garbanzo bean extracts show hepatoprotective activity in animal models, reducing liver enzyme markers (ALT, AST, ALP) and exhibiting antioxidant and anti-inflammatory effects in liver tissue. Their low glycemic index and fiber content also reduce hepatic fat accumulation relevant to non-alcoholic fatty liver disease (NAFLD), by reducing insulin spikes that drive hepatic lipogenesis.

• gardeniaScientific

  The liver is the best-documented organ target for Gardenia jasminoides. Evidence spans clinical studies showing bilirubin and transaminase reduction in jaundice, and multiple animal models of NAFLD, NASH, fibrosis, cholestasis, and drug-induced hepatotoxicity. Geniposide's hepatoprotective mechanism involves antioxidant, anti-inflammatory, and antifibrotic signaling.

• gardenia jasminoidesScientific

  Gardenia jasminoides has the most extensively documented organ-specific effects in the liver. Geniposide and crocins are hepatoprotective against chemical liver injury models (CCl4, ANIT, acetaminophen, alcohol), reduce fibrosis markers (α-SMA, collagen), lower ALT/AST, modulate hepatic CYP-450 enzymes, and promote biliary function. It is formally listed in the Chinese Pharmacopoeia for liver-biliary conditions.

• garlicScientific

  Multiple RCTs demonstrate garlic supplementation reduces hepatic steatosis in NAFLD patients and improves liver enzyme markers. A 15-week RCT found 51.1% of the garlic group achieved steatosis improvement versus 15.7% in placebo (RR 5.6). Garlic's organosulfur compounds, especially SAMC and allicin, reduce hepatic oxidative stress, lipogenesis, and NF-κB-driven inflammation.

• garlic bulbScientific

  Garlic supplementation has demonstrated hepatoprotective effects in NAFLD patients, reducing liver enzymes, hepatic steatosis, and oxidative stress. Multiple clinical studies support garlic's upregulation of hepatic detoxification enzymes. An RCT in NAFLD patients showed significant improvements in liver-related markers including fasting insulin, oxidative stress, and body composition.

• gastrodiaScientific

  Gastrodin and GE extracts protect against alcohol-induced, D-galactose-induced, and vancomycin-induced liver injury in animal models. Mechanisms include antioxidant enzyme upregulation, cytokine suppression, and PI3K/Akt pathway activation. GE is approved in China as a health food for liver protection.

• gentianScientific

  Gentian root has documented hepatoprotective activity in preclinical models, with G. asclepiadea extracts significantly reducing liver damage markers (ALT, AST, bilirubin) and restoring antioxidant enzyme levels (SOD, catalase, GSH) in CCl₄-injured rats. G. manshurica protected against alcohol-induced fatty liver. Choleretic use is endorsed by Commission E and the WHO monograph. Gentiopicroside mitigates chemical and alcohol-induced liver damage in cell and animal studies.

• gentian rootScientific

  Gentian species exhibit hepatoprotective activity in multiple animal models, reducing serum AST, ALT, ALP, and bilirubin, augmenting antioxidant enzymes, and protecting against chemically induced hepatocyte damage. Key active compounds are gentiopicroside, swertiamarin, and sweroside. In TCM, gentian ('Long Dan Cao') is a primary liver herb. A 2025 PMC review confirmed hepatoprotective mechanisms including CYP2E1 inhibition and liver fibrosis reduction. Human liver-specific clinical data are lacking.

• gentiana macrophyllaScientific

  Gentiana macrophylla and its active constituent gentiopicroside are hepatoprotective in multiple preclinical models, reducing ALT, AST, MDA, and hepatic inflammation. Mechanistically, gentiopicroside activates LKB1/AMPK pathways, reduces NLRP3 inflammasome activity, and restores hepatic architecture in chemical, alcoholic, immune, and lipotoxic liver injury models.

• gingerScientific

  Ginger has documented hepatoprotective effects supported by both animal studies and human meta-analyses. A meta-analysis found ginger supplementation significantly reduces alanine aminotransferase (ALT) and insulin resistance in nonalcoholic fatty liver disease (NAFLD). The mechanism involves reduction of oxidative stress and suppression of pro-inflammatory mediators in hepatic tissue.

• ginsengScientific

  Ginseng has documented hepatoprotective mechanisms acting on NAFLD and drug-induced liver injury through antioxidant enzyme upregulation, PI3K/AKT signaling, and the intestinal flora–liver axis. A meta-analysis of 14 RCTs found conventional doses do not significantly alter liver enzymes in healthy individuals, while clinical studies in NAFLD and chronic liver disease populations show benefit. NIH LiverTox notes ginseng reduces hepatic injury in animal models and is largely safe.

• glehnia littoralisScientific

  Hepatoprotective properties of G. littoralis are confirmed across the 2019 and 2023 systematic reviews and directly tested in HepG2 cell models. TCM prescriptions use it for hepatic fibrosis. A 2017 Korean study demonstrated protective effects against α-amanitin-induced hepatotoxicity in human hepatoma cells.

• glehnia rootScientific

  Hepatoprotective activity of G. littoralis is demonstrated in preclinical studies, and TCM formulas containing glehnia (notably Yi Guan Jian decoction) have been studied in rat models of liver fibrosis with positive outcomes. Evidence is animal-model based.

• glucomannanScientific

  The liver is a primary target organ of glucomannan's cholesterol-lowering mechanism: bile acid sequestration by glucomannan in the gut forces hepatic upregulation of LDL receptors to acquire cholesterol for new bile acid synthesis. Colonic SCFAs from glucomannan fermentation (propionate) also reach the liver via the portal vein and inhibit hepatic cholesterol and fatty acid synthesis.

• glycineScientific

  Glycine is produced primarily in the liver, serves as a rate-limiting GSH precursor for hepatic antioxidant defense, performs phase II detoxification conjugation, and directly cytoprotects hepatocytes via glycine-gated chloride channels on Kupffer cells. Human NAFLD liver transcriptomics show suppressed glycine biosynthetic genes, and glycine supplementation is under investigation as NAFLD/MASLD therapy.

• glycitinScientific

  Soy isoflavones are investigated for hepatoprotective effects in non-alcoholic fatty liver disease (NAFLD). A 2024 clinical study examined soy isoflavones' effects on NAFLD and FGF-21/fetuin A levels. Glycitin as a soy isoflavone constituent participates in hepatic lipid metabolism modulation via PPAR-γ activation. The WISH trial, which contained glycitin, also listed hepatic steatosis as a targeted condition in related patent literature.

• glycyrrhetinic acidScientific

  Glycyrrhetinic acid (GA), the primary bioactive metabolite of glycyrrhizin from licorice root, has well-documented hepatoprotective properties supported by multiple preclinical studies and clinical use of its parent compound. It acts via anti-inflammatory, antioxidant, anti-fibrotic, and choleretic mechanisms in the liver. Evidence covers cholestatic liver injury, NAFLD, drug-induced hepatotoxicity, and viral hepatitis, though robust isolated GA human RCTs remain limited compared to its precursor glycyrrhizin.

• glycyrrhizinScientific

  Glycyrrhizin, the principal bioactive triterpene of licorice root, has substantial clinical and preclinical evidence supporting hepatoprotective activity. Randomized controlled trials have demonstrated significant reductions in serum aminotransferases and histological improvement in chronic viral hepatitis patients. Glycyrrhizin-based preparations are approved and widely used adjunctive treatments for liver disease in Japan and China. Evidence spans viral hepatitis, drug-induced liver injury, NAFLD/NASH, and autoimmune hepatitis, though study quality and geographical concentration remain limitations.

• goji berryScientific

  Goji berry has well-documented hepatoprotective effects in both animal models and a human clinical study. A 45-day human RCT in metabolic syndrome patients showed significant reductions in AST and ALT (liver transaminases). Animal research demonstrates protection against alcohol-induced liver injury, CCl4 toxic hepatitis, and fatty liver disease, partly mediated through gut microbiota.

• goldensealScientific

  Berberine (goldenseal's main alkaloid) has been studied in clinical trials for non-alcoholic fatty liver disease (NAFLD) and liver protection, with ConsumerLab noting clinical evidence for NAFLD as one of berberine's proposed uses. The NCCIH cautions that poor bioavailability limits applicability to goldenseal supplements.

• gooseberryScientific

  Amla is classified as 'hepatoprotective' in multiple PubMed-indexed reviews. It enhances antioxidant defenses in human hepatocyte cell lines (HepG2), animal studies show reversal of liver damage, and the 2019 RCT measured liver hepatotoxicity markers as an efficacy endpoint.

• grapeScientific

  GSE supplementation has been tested in clinical trials specifically in NAFLD patients, with a double-blind RCT (520 mg/day, 2 months, n=50) measuring liver enzymes, hepatic steatosis, and metabolic factors. Animal studies confirm GSPE hepatoprotective effects against steatosis and lipid deposition. GSE modulates hepatic cholesterol metabolism genes (LDLR, CYP7A1, ABCG5/8) and reduces liver oxidative stress.

• grape seedScientific

  A double-blind RCT (n=50 NAFLD patients, 520 mg/day GSE for 2 months) found significant reductions in ALT, AST, LDL, triglycerides, insulin resistance, and steatosis markers versus placebo. A second double-blind RCT (200 mg twice daily, NAFLD patients) replicated these liver enzyme and lipid profile improvements. NIH/NCCIH acknowledges preliminary clinical research linking GSE to liver health benefits.

• grapefruitScientific

  Grapefruit's naringenin and naringin protect liver cells from oxidative stress and inflammatory injury, with evidence from a 36-study PRISMA systematic review demonstrating effects on NAFLD-related pathways. Grapefruit juice potently inhibits hepatic CYP3A4 and CYP1A2 enzymes, a well-documented pharmacological effect on liver drug metabolism. Animal and in vitro studies show naringenin reduces hepatic steatosis, VLDL overproduction, and NF-κB-driven hepatic inflammation.

• green chirettaScientific

  The liver is one of the primary target organs for green chiretta's pharmacological effects. Preclinical hepatoprotective evidence is extensive and mechanistically well-characterized; over 50% of Indian herbal liver formulations contain the herb. Clinical data from liver function monitoring in diabetic and gastroenterological patients support hepatoprotective benefit.

• green teaScientific

  Green tea, primarily via its catechin epigallocatechin gallate (EGCG), has clinical and meta-analytic evidence supporting a hepatoprotective role, particularly in nonalcoholic fatty liver disease (NAFLD). Multiple randomized controlled trials and meta-analyses report significant reductions in liver enzymes (ALT, AST) in NAFLD patients. However, evidence is mixed across broader populations, and high-dose green tea extract supplements have been associated with rare but documented liver toxicity.

• gymnema sylvestreScientific

  GS extracts demonstrate hepatoprotective activity in animal models by reducing elevated ALT, AST, ALP, and lipid peroxidation markers, restoring glutathione and SOD, and providing protection against D-galactosamine and paracetamol-induced hepatotoxicity. Traditional Ayurveda also classifies GS as a liver tonic.

• haliotisScientific

  Aqueous extracts of Haliotis shell (H. discus hannai, H. ruber, H. laevigata) demonstrated hepatoprotective effects in a carbon tetrachloride-induced mouse liver injury model, increasing liver glycogen, reducing portal inflammation, and promoting hepatocyte regeneration.

• hedychium spicatumScientific

  Hepatoprotective activity of H. spicatum is supported by in vitro and in vivo preclinical studies, including protection of hepatocytes from CCl4 toxicity, normalization of SGOT/SGPT, and amelioration of indoxacarb-induced liver damage in an in vivo feeding study. Ayurvedic tradition also uses the plant as a liver tonic.

• hesperetinScientific

  Hesperetin modulates hepatic cholesterol metabolism through inhibition of HMG-CoA reductase and ACAT enzymes, demonstrated in animal studies. It has documented positive effects on non-alcoholic fatty liver disease and is metabolized to active forms in the liver. Human RCT evidence is indirect via lipid biomarker modulation.

• hesperidinScientific

  Hesperidin protects the liver against oxidative damage, fibrosis, and toxin-induced injury. It maintains hepatic glutathione and catalase, inhibits activated hepatic stellate cells, suppresses NF-κB-driven hepatic inflammation, and reduces lipid accumulation in the liver. Evidence is robust in animal models; human clinical data are indirect (derived from lipid-lowering and CRP-reduction RCTs).

• hibiscusScientific

  A 12-week human RCT demonstrated Hibiscus sabdariffa extract improved liver steatosis in obese adults. Multiple animal studies confirm hepatoprotective effects via downregulation of lipogenic genes (SREBP-1c, PPAR-γ), reduction of liver enzyme markers, and attenuation of hepatic inflammation. Traditional use for liver disorders is globally documented.

• HMR (7-hydroxymatairesinol)Scientific

  In HFD-fed mice, HMR significantly reduced hepatic steatosis (by 62%) and modulated fat metabolism genes in liver tissue. Its metabolites also reduced triglyceride uptake in hepatoma cells in vitro. The liver is the primary site of HMR metabolism to enterolactone and also of its effects on estrogen-metabolizing enzymes (CYP450 pathways).

• HMR lignanScientific

  In a high-fat diet mouse model, HMRlignan reduced liver steatosis by 62%, indicating hepatoprotective effects against lipid accumulation. HMR metabolites enterolactone and enterodiol reduced TAG uptake in hepatoma cells in vitro. The liver is also the primary site of SHBG synthesis stimulated by enterolactone, contributing to hormone regulation.

• honeysuckleScientific

  L. japonica has documented hepatoprotective activity in preclinical models including CCl4-induced liver injury, dimethylnitrosamine-induced fibrosis, and NASH. Extracts reduce ALT, AST, MDA, and liver fibrosis while increasing GSH and hepatocyte survival. Pharmacokinetic studies confirm that active compounds reach and act upon the liver.

• hopsScientific

  Xanthohumol from hops has demonstrated hepatoprotective effects in animal models, preventing lipid oxidation, ameliorating high-fat-diet-induced hepatic injury, and reducing dysfunctional lipid and bile acid metabolism. The mechanism involves SREBP inhibition and antioxidant activity. Human liver data are not yet available from RCTs.

• horehoundScientific

  Animal and in vitro studies consistently demonstrate hepatoprotective activity of M. vulgare extracts, attributed to antioxidant polyphenols and a novel antihepatotoxic monoterpene acid. The PMC pharmacological overview classifies hepatoprotective effects among M. vulgare's most investigated properties. Traditional use for liver complaints is also documented by WebMD and EMA.

• hyacinth beanScientific

  Hepatoprotective effects of L. purpureus are documented in preclinical studies and metabolomics research. Animal models show liver protection consistent with known flavonoid and saponin mechanisms. Hyacinth bean administration attenuated HFD-induced hepatic lipid and bile acid metabolism dysregulation in a rodent metabolomics study.

• hydrangeaScientific

  In vitro studies have isolated hepatoprotective coumarins and secoiridoids from H. paniculata stems that showed activity against DL-galactosamine-induced toxicity in human HL-7702 liver cells (PubMed PMID 24811324). The secoiridoid sweroside in hydrangea root also shows hepatoprotective activity in separate models. Evidence is limited to cell culture; no animal or human liver studies have been conducted specifically with hydrangea.

• hydroxycitric acidScientific

  The liver is the primary site of HCA's metabolic action, as ATP-citrate lyase is most active in hepatic cells. HCA promotes hepatic glycogen synthesis, reduces de novo lipogenesis, and in NAFLD models reduces hepatic fat accumulation. Human RCTs in NAFLD patients confirm improvements in metabolic and some liver-related parameters.

• immortelleScientific

  H. italicum and closely related Helichrysum species have documented hepatoprotective and detoxifying properties in folk medicine, with in vitro and animal-level evidence supporting these effects. An MDPI 2026 study confirmed H. italicum extracts mitigated LPS-induced inflammatory gene expression specifically in liver cell lines.

• indian baelScientific

  Multiple controlled animal studies demonstrate that Aegle marmelos leaf and fruit extracts protect the liver against CCl4-induced, alcohol-induced, and H. pylori toxin-induced hepatotoxicity, restoring liver enzyme levels (ALT, AST, ALP, bilirubin) and hepatic antioxidant enzyme activity to near-normal levels.

• indian sarsparillaScientific

  Hepatoprotective activity is among the most robustly documented pharmacological properties of H. indicus, supported by PubMed-indexed animal studies showing liver enzyme normalization comparable to silymarin. The root extract also corrects hepatic cytochrome P-450 enzyme system dysregulation in diabetic rats.

• indian tinosporaScientific

  Hepatoprotection is among the most scientifically developed properties of T. cordifolia, supported by extensive preclinical data and limited human clinical trials. It protects against CCl4, lead, and anti-tuberculosis drug-induced hepatotoxicity. Mechanisms involve lipid peroxidation inhibition, antioxidant enzyme upregulation, anti-inflammatory alkaloid activity, and normalization of liver enzymes. Clinical trials for liver protection in tuberculosis patients have been reported.

• indigo leavesScientific

  Hepatoprotective activity of I. tinctoria leaf extracts is demonstrated in peer-reviewed animal studies showing significant restoration of liver enzymes (AST, ALT, ALP) and antioxidant parameters in chemically induced liver injury. Traditional use for liver conditions spans Ayurveda and TCM. Caution: higher doses of indigo naturalis have caused mild liver dysfunction in clinical trials.

• indole-3-carbinolScientific

  Indole-3-carbinol (I3C), a phytochemical from cruciferous vegetables, has documented preclinical (animal and cell) evidence for hepatoprotective effects across multiple liver disease models including alcohol-related liver injury, NAFLD/NASH, acute liver injury, and hepatic fibrosis. Its primary mechanism involves modulation of hepatic cytochrome P450 enzymes, anti-inflammatory, antioxidant, and anti-apoptotic activity. Human clinical evidence is currently limited; the body of evidence is predominantly preclinical.

• inositolScientific

  Inositol is a lipotropic agent required for hepatic VLDL assembly and triglyceride export; deficiency leads to hepatic fat accumulation in animal models. Clinical studies in obese NAFLD patients show myo-inositol improves insulin sensitivity, liver enzymes, and cardiometabolic markers. An RCT of pinitol in human NAFLD showed reductions in liver fat and AST.

• inula racemosaScientific

  Multiple preclinical studies demonstrate hepatoprotective activity of I. racemosa root extract in rodent models using paracetamol, CCl4, rifampicin, diethylnitrosamine, and ischemia-reperfusion injury, with effects comparable to silymarin. The bioactive sesquiterpene lactones (alantolactone, isoalantolactone) are identified as responsible constituents.

• inulinScientific

  Inulin-generated SCFAs, particularly acetate, act on hepatic free fatty acid receptor 2 (FFAR2) to improve insulin sensitivity in the liver and reduce hepatic steatosis. Clinical and preclinical evidence supports a role in reducing NAFLD-related hepatic fat accumulation via gut microbiota–bile acid–lipid metabolism pathways.

• isomalto-oligosaccharideScientific

  Animal studies show IMO prevents HFD-induced hepatic lipid accumulation and NAFLD-like pathology. IMO modulates liver metabolome associated with lipid metabolism. Human evidence is indirect; clinical trials show IMO reduces blood cholesterol and triglycerides, which reflect hepatic lipid processing.

• jiaogulanScientific

  Jiaogulan gypenosides protect the liver from NAFLD, oxidative injury, and lipid accumulation via PPARα activation, Nrf2 antioxidant signaling, and reduction of de novo lipogenesis. Both preclinical studies and limited human clinical trials in NAFLD support hepatoprotective activity.

• jujubeScientific

  Jujube demonstrates robust hepatoprotective activity across multiple preclinical models including alcohol-, APAP-, and CCl4-induced liver injury, acting primarily via Nrf2/ARE antioxidant pathway activation and NF-κB anti-inflammatory suppression. Multiple studies confirm reduced ALT, AST, ALP, and bilirubin. Traditional TCM classification as a liver tonic is supported by these mechanistic findings.

• kaleScientific

  Kale's sulforaphane activates hepatic Nrf2, inducing phase II detoxification enzymes (GST, NQO1, HO-1) that neutralize dietary carcinogens and xenobiotics. I3C from kale protects against liver fibrosis and injury in animal models. Kale has traditional use for hepatic disorders across multiple cultures.

• kudzuScientific

  Kudzu (Pueraria lobata) has a deep traditional Chinese medicine history of use for alcohol-related conditions, which extends to protection of the liver. Preclinical evidence—in vitro and rodent studies—demonstrates that its key isoflavones (puerarin, daidzin, daidzein) reduce liver enzyme markers (ALT, AST), suppress inflammatory pathways (TNF-α, NF-κB), and scavenge reactive oxygen species in models of chemically- and alcohol-induced hepatotoxicity. No robust human clinical trials specifically targeting liver outcomes have been published; human studies have focused primarily on alcohol intake reduction. A cautionary note exists: one study found high-dose kudzu root extract elevated AST/ALT in mice, suggesting dose-dependent hepatotoxicity is possible.

• L-alanineScientific

  The liver is the principal site of L-alanine catabolism and the organ most dependent on alanine as a gluconeogenic substrate. Hepatic alanine uptake is tightly regulated by insulin and glucagon, and the liver's capacity to convert alanine to glucose exceeds that of all other amino acids. L-alanine also activates hepatic AMPK, a key energy-sensing enzyme.

• L-alanyl-L-glutamineScientific

  AG protects the liver from oxidative stress, inflammation, and lipid accumulation in preclinical models of acute liver injury, NASH, and NAFLD. In LPS-induced acute liver injury in mice, AG reduced transaminases, hepatic apoptosis, and macrophage accumulation. In NAFLD and NASH mouse models, AG attenuated hepatic steatosis and fibrosis. Clinical data derive from perioperative IV AG studies impacting liver-related metabolic markers.

• L-asparagineScientific

  L-asparagine's hydrolysis product, aspartate, is an essential component of the hepatic urea cycle—the liver's primary pathway for detoxifying ammonia generated from amino acid catabolism. Aspartate is synthesized predominantly in the liver and participates in argininosuccinate synthesis, a key urea cycle step. This relationship is well-documented in peer-reviewed biochemistry; asparagine synthetase deficiency is also listed among hereditary disorders of L-aspartate metabolism.

• l-carnitineScientific

  The liver is a primary site of L-carnitine synthesis and utilization; it requires carnitine for fatty acid β-oxidation to prevent lipid accumulation. Clinical RCTs and meta-analyses show L-carnitine supplementation improves NAFLD severity, liver function tests, and hepatic encephalopathy in cirrhotic patients.

• L-cysteineScientific

  The liver is the organ most directly dependent on L-cysteine for glutathione-mediated detoxification. L-cysteine is the rate-limiting precursor for hepatic GSH synthesis, which drives Phase II detoxification. NAC is medically established for acetaminophen-induced acute liver failure. Evidence also supports a role in NAFLD via reduction of hepatic oxidative stress and inflammation.

• L-cystineScientific

  The liver is the primary organ of glutathione synthesis and relies on cysteine availability as the rate-limiting step. L-cystine is reduced intracellularly to cysteine for hepatic GSH production, which supports phase II detoxification and protects hepatocytes from oxidative damage. Animal and mechanistic human data support this role; direct L-cystine liver RCTs are limited.

• L-glutamineScientific

  The liver is a major site of glutamine catabolism and a key organ in ammonia detoxification via the urea cycle, for which glutamine is a nitrogen donor. In liver failure, impaired glutamine-ammonia homeostasis drives neurological and systemic complications, and the glutamine challenge test is a clinical diagnostic tool.

• L-glutathioneScientific

  L-glutathione (GSH) is the liver's primary endioxant and a key hepatoprotective molecule, with GSH deficiency documented as a pathological hallmark of both alcoholic and non-alcoholic liver disease. Human clinical studies, including an open-label multicenter pilot trial and a 2025 literature review of three RCT-eligible trials, consistently show that oral GSH supplementation reduces ALT levels and oxidative stress markers in NAFLD patients. Evidence is promising but currently limited by small sample sizes; large-scale RCTs are needed to confirm efficacy and determine optimal dosing.

• L-glycineScientific

  The liver is the primary site of glycine metabolism and the location where glycine performs its two major detoxification functions: glutathione synthesis and Phase II glycine conjugation of xenobiotics and bile acids. Preclinical data show glycine protects the liver from alcohol, acetaminophen, and ischemia-reperfusion injury, and small clinical trials suggest benefits in fatty liver and chronic hepatitis.

• L-leucineScientific

  The liver receives leucine from the portal circulation and uses it as a ketogenic substrate (yielding acetyl-CoA and acetoacetate), while leucine also stimulates hepatic protein synthesis via mTORC1. Elevated circulating BCAAs including leucine are associated with NAFLD and metabolic liver dysfunction, while exercise-driven reductions in leucine correlate with improved liver fat in clinical trials.

• L-methionineScientific

  The liver is the primary site of methionine metabolism; up to 50% of dietary methionine is processed hepatically. L-methionine is the precursor to SAMe, which maintains hepatic methylation and glutathione pools critical for lipid metabolism and detoxification. SAMe supplementation has been studied in 41 liver-disease trials, with evidence of benefit in alcoholic liver disease and cholestasis. Methionine deficiency exacerbates fatty liver and toxic liver injury.

• L-ornithineScientific

  L-ornithine is an obligate intermediate in the hepatic urea cycle, the primary pathway for detoxifying ammonia generated from amino acid catabolism. As LOLA, it is clinically used for hepatic encephalopathy in cirrhosis, with meta-analyses of 8+ RCTs confirming efficacy. Proposed mechanisms include direct ammonia-to-urea conversion, glutamine synthesis, glutathione upregulation, and NO-mediated improvement of hepatic microcirculation.

• L-threonineScientific

  L-Threonine plays a lipotropic role in the liver, supporting normal fat metabolism and preventing hepatic lipid accumulation. Animal studies consistently demonstrate that threonine deficiency causes fatty liver through impaired lipid transport mechanisms. Threonine is also catabolized in liver mitochondria to glycine, which participates in hepatic Phase II detoxification via glycine conjugation.

• L-valineScientific

  Patients with liver cirrhosis have decreased serum BCAA levels including valine, and BCAA-enriched supplementation is an established therapy for hepatic encephalopathy. A Cochrane systematic review of 16 RCTs found BCAAs had a beneficial effect on manifestations of overt hepatic encephalopathy (RR=0.73). A meta-analysis of 28 studies found oral BCAAs better than controls for preventing hepatic encephalopathy and liver-related events.

• lactobacillus caseiScientific

  L. casei Shirota has been studied for improving intestinal permeability in metabolic syndrome patients, directly reducing hepatic exposure to bacterial LPS—the primary driver of non-alcoholic fatty liver disease (NAFLD) pathogenesis. Mechanistically, L. casei's role in reducing endotoxemia and systemic inflammation is hepatoprotective. Indirect clinical evidence derives from metabolic syndrome RCTs.

• lactobacillus plantarumScientific

  L. plantarum supplementation has been linked to improved liver glycogen storage, favorable hepatic lipid metabolism changes, and reduction of liver-relevant metabolic parameters (cholesterol, triglycerides) across multiple RCTs. Preclinical evidence includes liver glycogen optimization in exercise models.

• lecithinScientific

  Phosphatidylcholine (PC) from lecithin is essential for hepatic VLDL secretion and fat export; PC deficiency causes hepatic steatosis. A double-blind RCT in TPN patients showed lecithin supplementation reduced fatty liver. Essential phospholipid preparations from soy lecithin have been studied clinically in Europe for alcoholic and non-alcoholic liver disease.

• lentinula edodes myceliaScientific

  LEM is well-documented in preclinical models to protect the liver against acute and chronic injury, reducing AST/ALT, suppressing fibrosis, and inhibiting collagen accumulation. Low-molecular-weight lignin fractions and phenolic acids (syringic, vanillic) are identified active components. Human evidence remains limited.

• licorice rootScientific

  Glycyrrhizin-based preparations have been used clinically in Japan for over 30 years to treat chronic viral hepatitis. Licorice significantly reduces liver enzymes (ALT, AST) and oxidative stress markers in preclinical models of alcohol-induced and diabetic liver disease. NIH LiverTox and multiple PMC reviews recognize licorice as an evidence-based hepatoprotective agent.

• lignansScientific

  The liver plays a central role in lignan metabolism: enterolignans absorbed from the colon enter hepatic portal circulation and undergo conjugation in the liver. The liver also mediates lignan effects on enterohepatic estrogen circulation, SHBG production, and lipid metabolism. Lignans have been shown to ameliorate oxidative stress in the liver in preclinical research.

• lilyScientific

  Easter lily (Lilium longiflorum) bulb extracts demonstrated significant hepatoprotective activity in a 24-week diabetic mouse study, reducing ALT, liver mass, triglycerides, and total cholesterol vs. diabetic controls. L. martagon bulbs have been used in European folk medicine specifically to treat liver disease. Preclinical evidence for hepatoprotective activity is supported by multiple in vivo studies.

• limoneneScientific

  D-limonene demonstrates hepatoprotective effects in multiple animal models including alcoholic and non-alcoholic fatty liver disease, reducing liver transaminase levels (ALT, AST), alleviating inflammatory infiltration, reducing lipid droplet accumulation, and modulating Phase I and Phase II detoxification enzymes. Antioxidant and NF-κB/Nrf2 pathway modulation underpin these effects.

• lion's maneScientific

  Lion's Mane polysaccharides protect the liver by strengthening the intestinal barrier to reduce LPS translocation, modulating the gut-liver axis, and increasing hepatic antioxidant enzymes. Animal models of NAFLD and alcoholic liver injury show hepatoprotective effects. NIH LiverTox confirms no liver toxicity associated with Lion's Mane use.

• liquid liver fractionsScientific

  Liver extract has a documented history of clinical use for hepatic dysfunction, with a 1975 double-blind RCT (Preziosi et al., n=40) showing 60% improvement in treated patients versus placebo on liver function parameters. Additional clinical reports suggest liver extract plus FAD may enhance interferon response in hepatitis C patients.

• lophatherum leafScientific

  Ethanol extracts of L. gracile leaf are hepatoprotective against CCl4-induced liver damage in mice, with reduced injury biomarkers. Flavonoids from the leaf protect against stress-induced liver injury in mice. Pharmacological reviews categorize hepatoprotective activity as one of the principal pharmacological effects of the herb's main constituents.

• lotus seedScientific

  Lotus seed and seedpod extracts protect hepatocytes from CCl4-, APAP-, LPS-, and lipotoxicity-induced injury in animal and cell studies, reducing ALT, AST, and improving lipid profiles. In TCM, lotus seeds indirectly support liver function through spleen-kidney tonification.

• luteolinScientific

  Luteolin, a polyphenolic flavonoid found in many vegetables and herbs, has been extensively studied in preclinical (cell and animal) models for hepatoprotective effects across multiple liver disease contexts—including NAFLD/MAFLD, alcoholic liver disease, hepatic fibrosis, ischemia-reperfusion injury, and hepatocellular carcinoma. Its mechanisms span anti-inflammatory, antioxidant, anti-lipogenic, and pro-apoptotic pathways in liver cancer cells. While it is noted as a key component of liver-protective drugs used in clinical practice (particularly in traditional Chinese medicine), large-scale independent human RCTs specifically for luteolin as a standalone agent are currently lacking.

• lycheeScientific

  Lychee pericarp polyphenols (epicatechin, procyanidin A2) have demonstrated significant hepatoprotective effects in CCl4-intoxication mouse models, reducing AST and ALT, preserving hepatocyte structure, and maintaining glutathione enzyme activities. Lychee peel extract also protects the liver in hyperuricemia models while allopurinol does not. In vitro, lychee flavanols suppress inflammatory mediators (iNOS, TNF-α) in hepatocytes.

• lycopeneScientific

  Lycopene accumulates in the liver and has been studied for hepatoprotective effects primarily in preclinical models. Animal studies demonstrate protection against LPS-induced hepatic injury via NF-κB suppression and oxidative stress reduction. Limited human data exist, but lycopene modulates hepatic lipid metabolism enzymes and antioxidant capacity.

• magnoliaScientific

  Magnolia bark extract activates the Nrf2 pathway in human hepatocytes, inducing antioxidant and detoxification enzymes. Magnolol protects against acute alcoholic liver damage via PI3K/Nrf2/PPARγ in animal models. A clinical study in NAFLD patients showed magnolia extract reduced hepatic fat content. Honokiol inhibits hepatic fat accumulation and NLRP3 inflammasome activation.

• maitake mushroomScientific

  Maitake supplementation in animal models inhibits hepatic lipid and cholesterol accumulation, modulates cholesterol metabolism gene expression in the liver, and may protect hepatocytes from lipid peroxidation. Traditional Chinese and Japanese medicine positioned maitake as a liver-protective tonic. No dedicated human hepatology RCTs exist.

• malabar nutScientific

  Hepatoprotective activity of vasicinone from A. vasica has been demonstrated in animal studies and confirmed in multiple pharmacological reviews. Traditional use includes jaundice treatment in Ayurveda. Antioxidant flavonoids further support liver protection.

• manganeseScientific

  The liver is the primary site of manganese uptake after absorption, and arginase—a manganese-containing hepatic enzyme—drives the urea cycle for ammonia detoxification. Excess manganese accumulates in the liver and can cause hepatotoxicity.

• mangoScientific

  A 12-week parallel RCT in overweight/obese adults found that daily mango consumption significantly reduced AST liver enzyme activity, a marker of hepatocyte stress, while total antioxidant capacity increased. In vitro and animal studies show mangiferin and other mango polyphenols reduce hepatic oxidative stress and inflammation.

• mangosteenScientific

  Multiple animal studies show α-mangostin protects against acetaminophen- and LPS/D-galactosamine-induced acute liver injury via Nrf2 activation and NF-κB suppression. Mangosteen peel extract prevented fibrosis in thioacetamide-induced liver injury models. A human RCT confirmed no hepatotoxicity (normal AST/ALT) after 30 days of mangosteen consumption, with measurable antioxidant improvements.

• maqui berryScientific

  In a rat metabolic syndrome model, maqui berry supplementation improved serum oxidative stress markers (MDA, SOD, carbonyls) relevant to hepatic oxidative load. The liver is a key site of glucose and lipid metabolism, and maqui's improvements in these parameters in human trials are consistent with hepatic benefit. No dedicated human liver study exists.

• marjoramScientific

  Marjoram extract has demonstrated hepatoprotective activity in a preclinical high-fat diet model, significantly correcting liver enzyme elevation (AST, ALT, GGT, ALP), reducing oxidative stress, and improving liver histology.

• mastic gumScientific

  Human and animal studies show mastic gum reduces liver enzymes (ALT, AST, ALP) and bilirubin in settings of hepatic dysfunction. The 18-month human study (5 g/day) showed significant reductions in AST, ALT, and ALP. A mouse NASH/fibrosis study demonstrated reduced ALT, improved hepatic steatosis, and reduced collagen content with mastic supplementation. Animal data confirm partial reversal of hepatic steatosis in diabetic models.

• MCT (medium chain triglycerides)Scientific

  The liver is the central metabolic site for MCT processing: medium-chain fatty acids are delivered directly via portal circulation, undergo rapid beta-oxidation, and generate acetyl-CoA and ketone bodies. The liver's role in MCT metabolism contrasts sharply with LCT processing, and excessive MCT intake can drive hepatic de novo lipogenesis, potentially elevating liver fat and serum triglycerides.

• methionine methylsulfonium chlorideScientific

  MMSC exerts hepatoprotective effects in multiple rodent models of chemically-induced liver injury, normalizing liver enzymes (ALT, AST, GGT, LDH), restoring antioxidant enzyme activity, and reducing histopathological damage. It participates in hepatic methionine-glutathione metabolism. All current evidence is preclinical.

• milk thistleScientific

  Milk thistle (Silybum marianum) and its active extract silymarin have been studied extensively in human clinical trials for liver disease, including alcoholic liver disease, hepatitis B/C, NAFLD/MASLD, and toxin-induced injury. Evidence from multiple RCTs and systematic reviews shows meaningful reductions in liver enzymes (ALT, AST) particularly in NAFLD, though results across other etiologies are mixed and no regulatory body has approved it as a liver treatment. Traditional use of the plant for liver and gallbladder disorders predates modern research by over 2,000 years.

• mintScientific

  Peppermint oil exerts choleretic effects via menthol's action on hepatic plasma membranes, stimulating bile secretion. Menthol inhibits β-D-glucuronidase binding in the liver, facilitating bile flow. Anti-inflammatory properties of menthol may also protect hepatic tissue from inflammatory damage.

• molybdenumScientific

  The liver is the primary site of expression for aldehyde oxidase and xanthine oxidase, both molybdenum-dependent enzymes central to phase I drug and toxin metabolism. A 2024 PMC review linked elevated XO and mARC to NAFLD, HCC, and liver fibrosis pathways. Sulfite oxidase deficiency also produces hepatic sulfite accumulation. The liver-molybdenum relationship is one of the most extensively described in the peer-reviewed literature.

• momordicaScientific

  Momordica charantia is documented in folk medicine for liver diseases and has preclinical evidence for hepatoprotective activity via antioxidant and anti-inflammatory mechanisms. Liver enzyme safety data from human RCTs show no hepatotoxicity. No human RCTs have specifically tested liver disease treatment.

• morindaScientific

  M. officinalis polysaccharides inhibit hepatic neutrophil and macrophage infiltration, protecting against hepatic injury. M. citrifolia reversed CCl4-induced liver damage in rats and reduced hepatic cholesterol, triglycerides, and improved hepatic antioxidant enzyme profiles (CAT, SOD, GPx) in obese hamsters. TCM classifies M. officinalis as acting on the liver meridian.

• morusScientific

  Mulberry anthocyanins and polyphenols exert hepatoprotective effects via Nrf2/MAPK pathway activation and antioxidant enzyme induction. The 2025 meta-analysis found mulberry supplementation improved AST in human trials. Preclinical evidence consistently demonstrates liver protection.

• mugwortScientific

  Hepatoprotective activity of A. vulgaris aqueous-methanol extract has been demonstrated in rodent models, with normalization of liver enzymes and reduction of oxidative hepatic damage. The plant inhibits HMG-CoA reductase in the liver and is listed in TCM for hepatitis. Multiple pharmacological reviews confirm hepatoprotective activity as established.

• mulberryScientific

  Mulberry flavonoids and anthocyanins protect liver cells from oxidative damage and lipid accumulation in cell and animal studies. A 2025 meta-analysis of 15 clinical RCTs found mulberry supplementation significantly improved AST levels. In vitro, mulberry leaf flavonoids protect HepG2 cells via Nrf2 activation.

• mustardScientific

  Mustard seed myrosinase enhances hepatic sulforaphane bioavailability, activating liver Nrf2 and phase II detoxification enzymes. Animal data show mustard seed extracts protect liver enzyme markers (AST, ALT, ALP) in diabetic models. Human RCTs confirm mustard myrosinase augments isothiocyanate delivery to liver-relevant pathways.

• myrobalanScientific

  TC water extract significantly attenuated drug-induced acute liver injury in mice, reducing AST, ALT, LDH, suppressing hepatic TNF-α/IL-1β/IL-6, and restoring antioxidant enzymes. Multiple animal models confirm hepatoprotection, including against anti-tuberculosis drug-induced liver toxicity.

• myrrhScientific

  Myrrh demonstrates hepatoprotective activity in multiple animal models, including reducing liver damage markers (AST/ALT) in sepsis models and ameliorating liver fibrosis in parasitic infection. The PMC pharmacological review confirms hepatoprotective properties. Myrrh sesquiterpene curzerene contributes antioxidant protection to liver tissue.

• NAC (N-acetyl cysteine)Scientific

  N-Acetyl Cysteine (NAC) has robust clinical evidence supporting its role in liver protection, most definitively as the standard-of-care antidote for acetaminophen (paracetamol)-induced hepatotoxicity. Its primary mechanism is replenishment of hepatic glutathione (GSH), which neutralizes toxic metabolites and counteracts oxidative stress. Clinical evidence also extends to drug-induced liver injury (DILI), acute liver failure from non-acetaminophen causes, alcoholic liver disease, and liver transplantation settings, though evidence strength varies across these indications.

• naringinScientific

  Naringin protects the liver from NAFLD, NASH, chemical-induced injury (CCl4, acetaminophen), and fibrosis in preclinical models by reducing lipid accumulation, suppressing NF-κB, activating Nrf2, and modulating gut microbiota. A 2025 multi-omics study confirmed hepatic lipid homeostasis restoration. Traditional TCM use of naringin-containing herbs for liver conditions supports historical context.

• nicotinamide ribosideScientific

  NR has direct relevance to hepatic health through its role as a hepatic NAD+ precursor. Post-hoc analysis of a 12-week human RCT in obese men using 2,000 mg/day NR suggested improvement in fatty liver, though primary metabolic endpoints were not improved. Preclinical evidence consistently demonstrates NR attenuates hepatic steatosis, fibrosis, and inflammation in NAFLD models via SIRT1/3 activation.

• NMN (β-nicotinamide mononucleotide)Scientific

  Animal studies show NMN restores hepatic NAD+ levels and improves liver fat metabolism, gluconeogenesis, and protection against steatosis. Human safety data confirm NMN does not adversely affect liver metabolic markers. Preclinical evidence is strong; dedicated liver endpoint human trials are lacking.

• nopalScientific

  Animal studies demonstrate nopal significantly attenuates hepatic steatosis, reduces hepatic triglycerides by approximately 50%, decreases liver injury biomarkers (ALT, AST), reduces hepatic oxidative stress, and improves liver insulin signaling. A 2023 PMC review confirmed consistent hepatoprotective effects of Opuntia preparations across multiple species and models. Human evidence is limited but includes hangover symptom reduction with an anti-inflammatory component.

• nut grassScientific

  Hepatoprotective activity of C. rotundus is confirmed in multiple animal studies, with significant protection against CCl4-induced hepatotoxicity at 100 mg/kg ethyl acetate extract. In TCM, the rhizome acts on the Liver channel. Both traditional and preclinical evidence consistently support liver-protective effects.

• okraScientific

  Okra exerts hepatoprotective effects via antioxidant enzyme induction, anti-inflammatory cytokine suppression, and lipid-lowering actions, confirmed in multiple animal models. A 2024 RCT in pre-diabetic adults found okra improved liver transaminase levels. Pectic polysaccharides from okra protected against CCl4-induced acute liver injury in mice.

• oleanolic acidScientific

  OA is a well-established hepatoprotective agent, officially listed as a liver-protective drug in China. It protects hepatocytes from chemical, drug-induced, and metabolic injury through antioxidant (Nrf2/HO-1) and anti-inflammatory (NF-κB/PPARα) mechanisms, reduces liver enzyme elevations, and inhibits liver fibrosis development.

• oliveScientific

  Olive oil added to a low-calorie diet improves NAFLD more effectively than diet alone. Hydroxytyrosol-rich and oleuropein-rich OLE demonstrated hepatoprotective effects in a rat NAFLD model, reducing liver enzymes and hepatic inflammation. Liver enzyme safety was assessed (unaffected) in the 12-week human insulin sensitivity RCT.

• olive oilScientific

  Olive oil, particularly EVOO, reduces hepatic fat accumulation (non-alcoholic fatty liver disease), improves liver enzymes, and protects hepatocytes from oxidative stress. Meta-analytic evidence from RCTs reports beneficial effects on alanine transaminase and hepatic fat mass with EVOO-enriched Mediterranean diet.

• omega-3 fatty acidsScientific

  Omega-3 PUFAs act directly on the liver to reduce hepatic lipid accumulation, inflammation, and oxidative stress in NAFLD/NASH. Meta-analyses of RCTs demonstrate significant reductions in liver enzymes (ALT, AST) and hepatic triglycerides with supplementation. Evidence is strongest for early-stage steatosis.

• omega-7 fatty acidsScientific

  Palmitoleic acid (omega-7) acts as a lipokine that reduces hepatic de novo lipogenesis and lipid accumulation. Preclinical studies in rodent models of NAFLD and diabetes show marked reduction in hepatosteatosis. The ongoing Harvard/BWH RCT (Frontiers in Endocrinology 2024) directly tests pure palmitoleic acid for hepatic lipogenesis reduction in overweight/obese prediabetic humans.

• omega-9 fatty acidsScientific

  Oleic acid (omega-9) at physiological dietary doses supports liver health by reducing hepatic steatosis, promoting fatty acid β-oxidation, and suppressing hepatic inflammation. Clinical and experimental data show OA contributes to improved hepatic enzyme profiles and reduced liver fat in metabolic disease contexts.

• onionScientific

  Onion demonstrates hepatoprotective activity through antioxidant, anti-inflammatory, and enzyme-normalizing mechanisms. Quercetin upregulates phase II hepatic detoxification enzymes and inhibits cytochrome P450 enzymes that activate hepatotoxins. Human RCT meta-analysis shows significant improvement in AST with onion supplementation.

• ophiopogonScientific

  Ophiopogonin D has demonstrated anti-NAFLD activity in preclinical research, and O. japonicus polysaccharide liposomes were shown to regulate liver immune (Kupffer) cell activity. Hepatoprotective effects are listed in pharmacological reviews of the plant's bioactive fractions.

• ophiopogon rootScientific

  Ophiopogonin D has documented anti-NAFLD (non-alcoholic fatty liver disease) activity in preclinical models, and O. japonicus oligosaccharides improve hepatic glucokinase activity and reduce hepatic lipid accumulation in diabetic rat models. These are preclinical findings with no human clinical liver trial data.

• orangeScientific

  Orange-derived hesperidin and flavonoids demonstrate hepatoprotective effects and improve liver lipid metabolism in pre-clinical and some clinical studies. Hesperidin reduces hepatic triglyceride and cholesterol accumulation, shows benefit in fatty liver models, and modulates PPAR pathways regulating hepatic lipid and glucose metabolism.

• oregon grapeScientific

  Berberine from Oregon grape has been evaluated in multiple RCTs for NAFLD with significant reductions in liver enzymes (ALT, AST, GGT) and hepatic fat content. A 2024 meta-analysis of 10 RCTs confirmed hepatoprotective effects. Traditional use of Oregon grape as a hepatic tonic for liver stagnation, jaundice, and hepatitis is extensive across multiple herbal traditions.

• oryzaScientific

  Rice bran (Oryza sativa) and its key bioactive gamma-oryzanol exert hepatoprotective effects, reducing liver fibrosis, oxidative stress, and inflammatory markers in animal models. Rice bran oil has been shown to reduce AST, ALT, and hepatic MDA while increasing glutathione in chemically-induced liver injury models.

• oyster mushroomScientific

  Pleurotus species show hepatoprotective activity in preclinical models, reducing elevated liver enzymes (ALT, AST), lipid peroxidation, and triglyceride accumulation in hepatocytes via antioxidant mechanisms. In human multi-outcome trials, oyster mushroom intake caused no adverse effects on liver function markers. Polysaccharide-peptides from golden oyster mushroom show in vitro hepatoprotective effects in NAFLD cell models.

• paederia foetidaScientific

  P. foetida is hepatoprotective in multiple rodent models, normalizing liver enzymes (ALT, AST, ALP) and activating the Nrf2/HO-1 pathway. The plant also inhibits cytochrome P450 enzymes CYP3A4 and CYP2D6, indicating hepatic metabolic interactions.

• palm oilScientific

  Palm tocotrienols have been studied in clinical trials for non-alcoholic fatty liver disease (NAFLD), with palm TRF shown to normalize hepatic echogenicity and prevent worsening of hepatic steatosis in a randomized controlled trial. Preclinical studies demonstrate TRF reverses hepatic steatosis, reduces liver inflammation, and protects against lipopolysaccharide-induced hepatic injury.

• palmitateScientific

  The liver is the primary storage organ for vitamin A palmitate (retinyl palmitate is the dominant hepatic storage form). Adequate hepatic vitamin A stores are essential for systemic distribution to target tissues including the retina and testis.

• palmitic acidScientific

  Palmitic acid is the central saturated fatty acid in hepatic lipotoxicity and NAFLD/MASLD pathogenesis. It induces hepatocyte lipid accumulation, mitochondrial dysfunction, oxidative stress, and inflammatory signaling, and impairs hepatic insulin sensitivity. A human breath-test study demonstrated that palmitic acid beta-oxidation is measurably reduced in NAFLD patients, reflecting impaired hepatic fatty acid disposal.

• palmitoleic acidScientific

  POA reduces hepatic lipid accumulation, suppresses liver inflammatory signaling, and modulates the gut-liver axis. Preclinical evidence is robust; a dedicated human RCT measuring hepatic lipogenesis via MRI spectroscopy is ongoing.

• pantethineScientific

  Pantethine is more efficient than pantothenate at raising hepatic CoA content, the rate-limiting cofactor for mitochondrial fatty acid oxidation in the liver. Studies show it activates multiple steps of hepatic fatty acid beta-oxidation and may reduce hepatic steatosis. Limited human biopsy data and multiple animal studies support a role in reducing fatty liver.

• papayaScientific

  Papaya seed extract has been studied for hepatoprotective effects in rat models of CCl4-induced liver injury, demonstrating reduction in oxidative stress, inflammation, and fibrosis markers. Papaya leaf extract also reduced hepatic viral RNA and inflammation in dengue mouse models. FPP has been shown to improve hepatic steatosis in diet-induced obese mice.

• parsleyScientific

  Parsley exhibits well-documented hepatoprotective effects in multiple animal models, reducing liver enzyme elevations, oxidative stress, and histological damage in toxic and diabetic conditions. Myristicin specifically induces hepatic glutathione S-transferase, enhancing phase II detoxification. Human liver studies are limited.

• peachScientific

  Peach kernel enters the Liver channel in TCM and is used for liver-related blood stasis conditions. In vitro studies show peach kernel inhibits hepatic stellate cell activation relevant to liver fibrosis. Polyphenol-rich peach extracts reduced hepatic steatosis in animal models.

• pearScientific

  Pear pomace water extract protected rats against high-fat-diet-induced hepatic lipid peroxidation and liver enzyme damage (ALT, AST), increasing hepatic antioxidative enzymes GPx and GST. Korean pear specifically stimulates alcohol dehydrogenase and aldehyde dehydrogenase, accelerating ethanol and acetaldehyde clearance — a traditional claim confirmed in vitro, in vivo, and in human trials.

• pectinScientific

  Pectin protects the liver by reducing hyperlipidemia-driven hepatic lipid accumulation, mitigating alcohol-induced liver injury by enhancing barrier-protective gut bacteria, and increasing liver FGF21 production that supports hepatic lipid oxidation and cardiac protection.

• peonyScientific

  Paeoniflorin demonstrates multiple hepatoprotective activities including protection against liver injury, cholestasis alleviation, liver fibrosis attenuation, NAFLD prevention, and antioxidant liver defense via Nrf2 and NF-κB pathways. These are documented across numerous animal and preclinical studies.

• perillaScientific

  Rosmarinic acid from Perilla has documented hepatoprotective effects, reducing liver injury markers in animal models. Perilla seed oil is described in clinical reviews as having hepatoprotective properties, and the lipid-lowering effects of ALA reduce hepatic lipid accumulation relevant to fatty liver disease.

• phellodendron amurenseScientific

  Berberine from P. amurense is hepatoprotective, inhibiting liver gluconeogenesis, stimulating bile secretion and bilirubin discharge, and protecting against chemical-induced hepatotoxicity in rodents. P. amurense is indicated in TCM for liver heat, jaundice, and hepatitis. WebMD notes berberine in phellodendron 'may protect the liver.' Traditional use for cirrhosis is also documented.

• phosphatidylcholineScientific

  Phosphatidylcholine (PC), particularly as polyenyl/essential phospholipids (EPL/PPC), has well-documented hepatoprotective effects supported by multiple human clinical studies. Its primary mechanism involves enabling hepatic VLDL synthesis and triglyceride export, reducing steatosis, and exerting anti-inflammatory and antifibrotic effects. Clinical trials and large observational studies demonstrate significant reductions in liver enzymes (ALT, AST, GGT) in patients with non-alcoholic fatty liver disease (NAFLD/MAFLD). Evidence is considered moderate in strength, with most studies being observational or open-label rather than large placebo-controlled RCTs.

• phyllanthusScientific

  Multiple species within the Phyllanthus genus (notably P. amarus, P. niruri, P. urinaria) have demonstrated hepatoprotective activity in preclinical studies and have been evaluated in human clinical trials, primarily for chronic hepatitis B virus (HBV) infection. Key bioactive lignans—phyllanthin and hypophyllanthin—are proposed to protect hepatocytes via antioxidant, anti-inflammatory, and antiviral mechanisms. Human clinical evidence exists but remains inconsistent, with Cochrane-level reviews concluding that high-quality evidence to definitively support use is still lacking. Phyllanthus species also carry a deep traditional background in Ayurveda, Traditional Chinese Medicine, and Amazonian folk medicine as a liver remedy.

• phytosterolsScientific

  Phytosterols influence liver metabolism by activating liver LXRα transcription factor, modulating LDL receptor expression, and reducing hepatic VLDL and TG production. A pilot human study in NAFLD patients showed a 19% relative reduction in liver steatosis with 2 g/day phytosterols over one year, alongside improvements in TG and CRP.

• picrorhiza kurroaScientific

  Picrorhiza kurroa (Kutki) has both documented Ayurvedic traditional use and peer-reviewed clinical evidence supporting its hepatoprotective role. Its active iridoid glycosides—picroside I and picroside II—are the primary agents responsible for protecting liver cells against toxic, inflammatory, and fatty injury. A randomized, double-blind, placebo-controlled human trial demonstrated significantly faster normalization of bilirubin and liver enzymes in acute viral hepatitis patients treated with P. kurroa versus placebo. Animal studies further show reversal of fatty infiltration in NAFLD models, outperforming silymarin at higher doses.

• pistacia integerrima gallScientific

  P. integerrima extracts have demonstrated hepatoprotective and hepatocurative effects in CCl4-induced liver injury rat models (Khan et al., 2004; combination study with Berberis lycium and Galium aparine). Traditional Ayurvedic formulations use the galls for 'yakrit roga' (liver disorders) and hepatitis. The 2020 comprehensive review identifies hepatoprotective activity as confirmed.

• plant sterolsScientific

  The liver is a key site of plant sterol action. By reducing intestinal cholesterol absorption, plant sterols upregulate hepatic LDL receptors and alter hepatic VLDL secretion. In subjects with elevated triglycerides, plant stanols have been specifically shown to reduce hepatic VLDL production, lowering circulating TG. The relationship with non-alcoholic fatty liver disease is under investigation with limited clinical data.

• plantainScientific

  A randomized double-blind clinical trial found P. major seed supplementation (2 g/day, 12 weeks) significantly reduced liver enzymes ALT and AST in NAFLD patients. P. major extracts showed hepatoprotective effects in in vitro models (protection of HepG2 cells and liver mitochondria from oxidative stress). Ursolic acid and oleanolic acid from P. major have documented hepatoprotective activity.

• platycodonScientific

  Platycodon root has well-documented hepatoprotective effects across multiple animal models including NAFLD, acute liver injury, and liver fibrosis. Reductions in ALT, AST, hepatic lipid accumulation, and fibrosis markers are consistently observed. PG saponins and polysaccharides are the primary active fractions.

• platycodon rootScientific

  Platycodon root and its primary saponin platycodin D exhibit hepatoprotective effects across alcohol-induced, endotoxin-induced, chemotherapy-induced, and diabetic liver injury models. Mechanisms include NF-κB and oxidative stress suppression, reduction of serum ALT/AST, and prevention of hepatic fibrosis. Multiple independent animal studies and liver-specific pharmacological reviews confirm this relationship.

• policosanolScientific

  Human RCTs have shown that policosanol supplementation significantly reduces liver enzymes ALT, AST, GGT, and ALP, markers of hepatic stress or damage. A 12-week placebo-controlled double-blind RCT in Japanese participants demonstrated ALT reduction of up to 21% and GGT reduction of 16%. Animal studies further document hepatoprotection against chemically induced liver injury and high-fat diet hepatotoxicity.

• polyporusScientific

  The liver is a major evidence-supported target of P. umbellatus. PUPS is an SFDA-approved pharmaceutical in China for hepatitis B treatment, with over 10,000 documented clinical cases, and preclinical data confirm hepatocyte regeneration, anti-fibrotic, and antioxidant hepatoprotective mechanisms.

• pomegranateScientific

  A double-blind, placebo-controlled RCT of pomegranate peel extract in NAFLD patients showed significant improvements in body weight, liver enzymes, and metabolic parameters. Preclinical data show pomegranate juice has hepatoprotective effects against paracetamol-induced acute liver damage. Pomegranate modulates hepatic lipid metabolism.

• pomeloScientific

  Pomelo coumarins protect human hepatic cell lines (LO2 cells) from D-galactosamine-induced injury by reducing ALT/AST and boosting SOD and GSH-Px. Pomelo peel powder prevents hepatic inflammation and fibrosis in CCl4-treated rats. A 2026 Nature journal study confirmed pomelo peel extract equivalently alleviates hepatic steatosis and oxidative stress in a diet-induced animal model.

• prickly pear cactusScientific

  Multiple preclinical studies and a human hepatocyte cell study confirm Opuntia extracts reduce hepatic triglyceride accumulation, suppress ALT/AST, and protect against oxidative liver damage via betalains and phenolics. A human clinical study showed hangover symptom reduction. Animal studies show hepatoprotection against multiple toxins.

• privetScientific

  Hepatoprotective effects are among the most studied and replicated properties of Ligustrum lucidum in preclinical research, attributed primarily to oleanolic acid increasing hepatic glutathione regeneration. In vitro and rodent studies show protection against oxidative, toxic, and mitochondrial hepatic injury. Preliminary human-level evidence exists via combination formula studies.

• propionic acidScientific

  Propionate reaches the liver via portal circulation and acts as a gluconeogenic substrate and regulator of hepatic lipid metabolism. It suppresses hepatic lipogenesis via GPR43/AMPK activation, reduces liver triglyceride accumulation, and inhibits cholesterol synthesis in hepatocyte models. Long-term colonic propionate delivery in overweight humans significantly reduced intrahepatocellular lipid content, and propionate has shown benefit in alcohol-related liver disease models.

• prunusScientific

  Prunus domestica extracts have documented hepatoprotective activity in preclinical models and in-vitro studies. A 2025 study used P. domestica subsp. syriaca extract in human steatotic hepatocytes (MASLD model) and showed beneficial effects on oxidative stress, lipid accumulation, and glucose metabolism pathways. Animal studies confirm fiber-rich P. domestica extract ('Prunophyte') reduces hepatic damage markers.

• pterocarpus marsupiumScientific

  Preclinical studies demonstrate that P. marsupium stem bark and leaf extracts protect the liver against chemical-induced injury, normalizing liver enzymes and improving hepatic histology. Effects are comparable to silymarin at appropriate doses.

• puerarinScientific

  Puerarin, the principal isoflavone glycoside from Pueraria lobata (kudzu root), has well-documented hepatoprotective properties supported by extensive preclinical research and emerging clinical trial data. It acts through multiple mechanisms including antioxidant defense, anti-inflammation, lipid metabolism regulation, and modulation of apoptosis and autophagy. The strongest evidence base comes from animal models of alcoholic liver disease, NAFLD/MASLD, and drug-induced liver injury, with clinical trials of puerarin-containing TCM formulas showing efficacy in NAFLD and insulin resistance. Large-scale monotherapy RCTs in humans are currently lacking.

• pumpkinScientific

  Pumpkin seed flour and oil have demonstrated hepatoprotective effects in animal models of dyslipidaemia and metabolic syndrome, reducing hepatic lipid accumulation and liver enzyme elevations. Human data show improved liver function markers with PSO supplementation. The mechanisms involve antioxidant activity and modulation of lipid metabolism.

• punarnavaScientific

  Multiple preclinical studies confirm hepatoprotective activity of B. diffusa against chemical liver injury (CCl4, paracetamol, alcohol), with significant reductions in ALT, AST, ALP, bilirubin, and histopathological preservation of liver tissue. A hydroalcoholic extract showed 70–80% hepatoprotection vs silymarin's 80–90% in rat models. Traditional use for jaundice, hepatitis, and liver cirrhosis is extensive.

• purslaneScientific

  Two double-blind RCTs in NAFLD patients demonstrate purslane significantly reduces liver enzymes (ALT, AST, GGT) from baseline and improves lipid and antioxidant profiles. In vitro studies confirm hepatoprotective activity. Traditional use of purslane for liver disorders is globally documented across Asian, European, and Middle Eastern medicine.

• quercetinScientific

  Quercetin is a dietary flavonoid with well-documented hepatoprotective properties in preclinical models, acting via antioxidant, anti-inflammatory, and antifibrotic mechanisms. Human clinical evidence is emerging but limited: at least one randomized, double-blind, placebo-controlled crossover trial demonstrated that 500 mg/day for 12 weeks modestly reduced intrahepatic lipid content in NAFLD patients. The NIH LiverTox database confirms broad in vitro and in vivo hepatoprotective data, while cautioning that robust prospective human trials remain sparse.

• quillajaScientific

  In a Wistar rat model, Quillaja bark saponin significantly protected against iron-induced hepatotoxicity, reducing liver enzyme elevations (ALT, AST, ALP, GGT) and improving antioxidant markers. The hepatoprotective mechanism involves reduction of oxidative stress and suppression of NOS expression. Evidence is preclinical only.

• radishScientific

  Radish has the strongest body of preclinical evidence for liver protection among its organ-level effects. Multiple animal studies confirm reductions in ALT/AST, lipid peroxidation, and liver histopathological damage via Nrf2/HO-1 antioxidant activation. A human pilot study showed Spanish black radish supplementation upregulated liver phase I and II detoxification enzymes.

• red yeast riceScientific

  RYR has a dual relationship with the liver: it shows preclinical and clinical evidence of benefit in non-alcoholic fatty liver disease (NAFLD) and liver cirrhosis prevention, yet the FDA, EFSA, and NIH LiverTox all document a risk of drug-induced liver injury (DILI) from RYR—particularly from high-monacolin-K or citrinin-contaminated products. Meta-analyses of RCTs show no significant liver enzyme abnormalities at standard doses, but multiple clinical case reports of hepatotoxicity exist.

• rehmanniaScientific

  Rehmannia demonstrates hepatoprotective effects in multiple preclinical models, including NAFLD, hepatic steatosis, and drug-induced hepatotoxicity. Catalpol activates AMPK/TFEB to reduce liver fat; ajugol mitigates NAFLD via autophagy-lysosome enhancement; and catalpol protects against triptolide hepatotoxicity via CAR/Nrf2 modulation. The herb is traditionally prescribed for liver yin tonification.

• rehmannia glutinosaScientific

  Rehmannia demonstrates hepatoprotective effects in multiple animal models of liver injury, including CCl4-induced hepatotoxicity and LPS-induced acute liver injury. Raffinose oligosaccharides significantly reduced ALT, AST, cholesterol, and TG in chemically-injured mice. Anti-inflammatory and antioxidant mechanisms protect hepatocytes.

• reishi mushroomScientific

  MSKCC lists hepatoprotective properties among reishi's established in vitro and in vivo findings. Multiple preclinical studies demonstrate antioxidative, anti-inflammatory, and lipogenic gene-suppressing effects in liver tissue. A 2025 PMC review identified NF-κB, Nrf2, and NLRP3 as core hepatoprotective signalling targets. TCM classified reishi as a liver tonic. Rare cases of clinical hepatotoxicity with reishi products are documented by NIH LiverTox.

• resveratrolScientific

  Resveratrol, a polyphenol found in grape peel, berries, and red wine, has been studied clinically for its potential to support liver health, particularly in non-alcoholic fatty liver disease (NAFLD). Multiple meta-analyses of randomized controlled trials exist, though results are inconsistent: subgroup analyses show improvements in liver enzymes (ALT, GGT) in patients with liver disorders, while overall pooled analyses often fail to reach statistical significance. Preclinical evidence is stronger, demonstrating reductions in hepatic steatosis, fibrosis, and inflammation via AMPK/SIRT1 signaling, but clinical translation remains limited and inconclusive.

• rhubarbScientific

  Rhubarb has documented hepatoprotective activity in clinical studies, reducing liver enzymes (ALT, AST), hepatic fat, and fibrosis markers. A 232-patient clinical trial using a rhubarb-containing formula for non-alcoholic fatty liver disease showed significant ALT reduction. TCM use for liver and biliary diseases is extensively documented.

• rhubarb rootScientific

  Rhubarb root is used clinically in Asian countries for chronic liver disease, jaundice, and hepatitis. Preclinical data confirm antifibrotic, anti-inflammatory, and antioxidant effects on hepatic tissue. The anthraquinone emodin is identified as the primary hepatoprotective constituent.

• robusta coffeeScientific

  Both caffeine and chlorogenic acids—the dominant bioactives in robusta coffee—have documented hepatoprotective effects. A direct comparison study in type-2 diabetic rats found robusta coffee reduced liver triglyceride content and modulated hepatic gene expression (G6pc, mTOR). Prospective cohort data link habitual coffee intake to reduced liver enzyme levels (ALT, GGT), lower incidence of chronic liver disease, and reduced hepatocellular carcinoma risk.

• roseScientific

  Rosehip (Rosa canina) has demonstrated hepatoprotective properties in pre-clinical models, with its antioxidant and anti-inflammatory constituents protecting against chemically induced liver damage. A 2024 PMC review of Rosa canina highlighted hepatoprotective effects among its documented properties. Traditional Persian medicine uses rose to cool the liver.

• rosmarinic acidScientific

  Rosmarinic acid has extensively documented hepatoprotective activity in preclinical models, protecting against CCl4-induced hepatotoxicity, cholestasis, NAFLD, and LPS/D-galactosamine-induced liver injury via Nrf2 pathway activation, NF-κB suppression, lipid peroxidation inhibition, and apoptosis prevention. A dedicated 2019 review (PMID 30780110) comprehensively characterizes RA as a hepatoprotective agent.

• royal jellyScientific

  Animal studies show RJ protects the liver from drug-induced hepatotoxicity (azathioprine, oxymetholone, diclofenac) and improves liver enzymes. A 2023 meta-analysis of 10 RCTs found no significant overall effect on liver enzymes (AST, ALT, ALP) in humans. Hepatoprotective evidence is primarily preclinical.

• rubia cordifoliaScientific

  Rubiadin, isolated from R. cordifolia, demonstrated hepatoprotective activity comparable to silymarin in CCl4-induced liver injury rats, reducing MDA and preserving glutathione dose-dependently. Additional studies confirm activity against acetaminophen-induced hepatotoxicity. Ayurveda and Unani medicine both prescribe it for liver disorders including jaundice.

• rutinScientific

  Rutin is extensively studied for hepatoprotective activity in animal models. It activates Nrf2/HO-1 and modulates NF-κB to protect hepatocytes, and has been shown to protect against cholestatic, drug-induced, and oxidative liver injury. A 2025 systematic review in Basic & Clinical Pharmacology & Toxicology comprehensively analyzed these mechanisms.

• saccharomyces boulardiiScientific

  A 2024 systematic review of 6 RCTs found S. boulardii reduced severity of cirrhosis manifestations, lowered Child–Pugh scores, and reduced pro-inflammatory cytokines (TNF-α, IL-1β, IL-6). Preclinical and a small human study support benefit in NAFLD via the gut–liver axis. The evidence base includes human RCTs, though study sizes are modest.

• safflowerScientific

  Safflower's HSYA has documented hepatoprotective effects including reduction of alcohol-induced liver fibrosis, alleviation of hepatic steatosis, and protection against ischemia-induced liver damage. Histological studies show alcohol-induced liver fibrosis is significantly reduced by HSYA through MAPK inhibition and TGF-receptor downregulation. Quercetin and kaempferol in safflower alleviate hepatic steatosis by upregulating NR1H4. A comprehensive clinical review confirms safflower's use for hepatobiliary conditions in clinical practice.

• saffronScientific

  Saffron and its constituents exert hepatoprotective effects supported by human RCTs, demonstrating reductions in liver enzymes (ALT, AST, ALP) in T2DM and NAFLD patients. Traditional Tibetan and Persian medicine recorded saffron's use for 'all liver diseases.' Saffron-based hepatic formulations are currently used in clinical settings in China and other regions.

• sageScientific

  Human clinical trials show sage extract does not cause hepatotoxicity and in some contexts normalizes elevated liver enzymes (AST, ALT) in diabetic patients. Animal studies show reduced hepatic lipid accumulation and improved liver glycogen. Sage's antioxidant polyphenols protect liver cells from oxidative stress.

• salvianolic acidScientific

  Salvianolic acids — especially the B and A isoforms — are water-soluble polyphenols from Salvia miltiorrhiza (Danshen) with well-documented hepatoprotective and anti-fibrotic activity supported by both preclinical and human clinical data. Mechanistically, they suppress hepatic stellate cell (HSC) activation, inhibit TGF-β/Smad and MAPK pro-fibrotic signalling, and reduce oxidative stress in liver tissue. A double-blind randomised clinical trial in chronic hepatitis B patients demonstrated that oral salvianolic acid B reversed liver fibrosis at a rate comparable to or exceeding interferon-gamma. Traditional Chinese medicine use of Danshen for liver and blood-stasis conditions provides additional historical context.

• SAMe (S-adenosyl-L-methionine)Scientific

  SAMe (S-Adenosyl-L-Methionine) is a naturally occurring molecule whose hepatic synthesis is depressed in chronic liver disease, providing a rationale for supplementation. It functions as the principal methyl donor and a precursor to glutathione, supporting antioxidant defense and membrane integrity in the liver. Multiple RCTs and systematic reviews confirm benefits in intrahepatic cholestasis and alcoholic liver disease, though evidence for hard clinical endpoints (mortality, transplant) remains limited. Overall, SAMe shows clinically meaningful improvements in liver function biomarkers and cholestatic symptoms, but the absence of large high-quality trials constrains definitive conclusions.

• sarsaparillaScientific

  Hepatoprotection is one of the four primary pharmacological functions of Smilax glabra rhizome per PMC-published reviews. Multiple preclinical studies show protection against liver injury and oxidative hepatic damage. Resveratrol, oxyresveratrol, and flavonoids are the key active compounds. MSKCC confirms hepatoprotective properties in preclinical research. No human liver trials exist.

• schisandraScientific

  Schisandra has the strongest scientific support for liver protection. Its lignans (schisandrin, gomisins) reduce hepatic inflammation, lower ALT/AST enzymes, enhance glutathione synthesis, modulate CYP450 enzymes, and promote hepatocyte regeneration. Small human trials in hepatitis B, hepatitis C, and NAFLD show improved liver enzymes and symptoms. A 2025 Frontiers in Pharmacology systematic review and meta-analysis consolidated preclinical and human data confirming hepatoprotective mechanisms.

• schisandrinsScientific

  Schisandrins — the dibenzocyclooctadiene lignans (principally Schisandrin A, Schisandrin B, and Schisandrin C) isolated from Schisandra chinensis — have well-documented hepatoprotective activity supported by both preclinical and limited human clinical evidence. Key mechanisms include upregulation of hepatic glutathione (GSH), modulation of cytochrome P450 enzymes (CYP3A, CYP2E1), inhibition of NF-κB-mediated inflammation, and activation of the Nrf2/HO-1 antioxidant pathway. Clinical data, though modest in scale, show reductions in ALT and AST in patients with viral hepatitis, drug-induced liver injury, and nonalcoholic fatty liver disease. Traditional Chinese Medicine has employed Schisandra chinensis for liver deficiency syndromes for centuries, providing a historical foundation that modern pharmacology has begun to substantiate.

• sclerotiumScientific

  Poria cocos polysaccharides are well-evidenced hepatoprotective agents in preclinical models of alcoholic liver disease, NASH, and acute liver failure, acting via Nrf2 antioxidant activation and NF-κB/TLR4 anti-inflammatory pathways. A Poria cocos polysaccharide oral solution is approved in China for hepatitis treatment.

• scrophularia rootScientific

  Hepatoprotective activity is one of the most consistently documented pharmacological properties of Scrophularia root in preclinical research. In vitro hepatoprotection is demonstrated for both S. ningpoensis and S. buergeriana root extracts. The compound angoroside C specifically exhibits hepatoprotection. Traditional TCM use also links the root to liver-clearing functions.

• secoisolariciresinol diglucosideScientific

  SDG protects the liver from diet-induced steatosis, chemical toxin–induced injury, and ER stress by reducing hepatic TG and cholesterol accumulation, activating antioxidant Nrf2 pathways, and normalizing lipid metabolic gene expression. Animal studies across multiple models confirm significant hepatic lipid normalization with 12 weeks of SDG. SDG is also hepatoprotective against ALT/AST elevation in systemic disease models.

• seleniumScientific

  Selenium has a well-documented, scientifically evidenced relationship with the liver. The liver is the primary organ for selenium metabolism and selenoprotein synthesis, and selenium deficiency is consistently observed in patients with chronic liver disease. Key selenoproteins (GPX1, TXNRD1, SELENOP) protect hepatocytes against oxidative stress-driven damage, while clinical and epidemiological studies link lower selenium status to more advanced liver fibrosis and worse outcomes in conditions such as NAFLD/MASLD and cirrhosis. The dose-response relationship is complex, however, as both deficiency and excess selenium carry hepatic risks.

• selenomethionineScientific

  The liver is the primary site of selenoprotein biosynthesis and selenium metabolism, with selenomethionine serving as the main substrate. Hepatic GPX activity is a key marker of selenium status, and SeMet supplementation increases selenoprotein biosynthesis in the liver, reducing CRP production and attenuating inflammatory processes. Preclinical studies show SeMet protects against chemically-induced hepatic oxidative injury and inflammation via GPX1 upregulation and NF-κB suppression.

• sesameScientific

  Sesame's hepatoprotective effects are among the most consistently documented in the literature. Sesamin restores liver enzymes and detoxification capacity after oxidative injury. Sesamolin inhibits hepatic lipid peroxidation. Animal studies show sesame oil protects against CCl4-induced liver fibrosis and enzyme elevation. Multiple clinical meta-analyses include liver enzyme improvements as outcomes. TCM has long used black sesame for liver nourishment.

• shiitake mushroomScientific

  Lentinan inhibits hepatic fat accumulation and protects against hepatotoxicity. Vitamin D-enriched shiitake extracts significantly reduced liver injury markers (ALT, AST) and improved histology in immune-mediated hepatitis mouse models. Eritadenine modulates hepatic cholesterol processing. Authors of the hepatoprotective study suggested potential use for HCV and NASH.

• sichuan pepperScientific

  Z. bungeanum extracts and amides demonstrate hepatoprotective and anti-NAFLD effects in multiple rodent models, with mechanisms including Nrf2 antioxidant pathway activation, ALT/AST normalisation, and modulation of hepatic lipid accumulation. Evidence is exclusively preclinical.

• silk treeScientific

  A. julibrissin shows hepatoprotective properties in preclinical research, with modulation of liver enzyme activity and protection from oxidative hepatic injury. TCM classifies it as entering the Liver meridian and uses it to free Liver qi stagnation.

• silybinScientific

  Silybin (the principal bioactive flavonolignan of milk thistle, Silybum marianum) has substantial human clinical evidence supporting hepatoprotective effects. Multiple randomized controlled trials and systematic reviews demonstrate reductions in liver enzyme levels (ALT, AST, GGT) across conditions including NAFLD/MASLD, alcoholic liver disease, and drug-induced liver injury. Mechanistically, silybin acts via antioxidant, anti-inflammatory, and antifibrotic pathways. Evidence is promising but varies by condition and formulation, and larger, well-designed RCTs are still needed for definitive conclusions.

• silybumScientific

  Silybum marianum (milk thistle) has an extensive body of human clinical research supporting its use for liver health, making it one of the most studied botanical hepatoprotectives. Its seed extract, silymarin, exhibits antioxidant, anti-inflammatory, and antifibrotic properties relevant to multiple liver conditions. However, while laboratory and animal evidence is strong, clinical trial results in humans have been promising but largely inconclusive due to methodological limitations. A 2023 systematic review of 29 RCTs found that silymarin reduced liver enzyme levels in the majority of trials, with the clearest benefit seen in non-alcoholic fatty liver disease.

• silymarinScientific

  Silymarin, a flavonoid complex from Silybum marianum (milk thistle), has substantial human clinical evidence supporting hepatoprotective effects in chronic liver diseases including NAFLD, alcoholic liver disease, and cirrhosis. Multiple randomized controlled trials and meta-analyses demonstrate significant reductions in liver enzymes (ALT, AST). However, evidence quality is mixed: effects on hard clinical outcomes (mortality, histology) are less convincing than biochemical improvements, and benefits for hepatitis C are not established with oral administration.

• sitostanolScientific

  Plant stanols including sitostanol reach the liver via chylomicrons and influence hepatic cholesterol metabolism. Animal and mechanistic studies show stanol esters reduce hepatic cholesterol ester content and decrease VLDL-cholesterol secretion from the liver. The proposed mechanism for triglyceride lowering by sitostanol involves decreased hepatic production of large, triglyceride-rich VLDL-1 particles.

• skullcapScientific

  Baicalin from S. baicalensis has documented hepatoprotective effects against viral hepatitis, fatty liver disease, xenobiotic liver injury, cholestasis, and hepatocellular carcinoma in preclinical models. In rats, baicalin (5 mg/kg i.p.) significantly reduced liver enzymes ALT and AST following chemically induced hepatotoxicity. S. baicalensis is used clinically in China for liver disease.

• smartweedScientific

  Hepatoprotective activity is categorized among the documented pharmacological activities of P. hydropiper in peer-reviewed literature. The plant's flavonoids and polyphenols reduce hepatic oxidative stress and inflammatory markers in preclinical models. Traditional use for liver enlargement is documented in Indian folk medicine.

• smilaxScientific

  Multiple Smilax species demonstrate hepatoprotective activity in animal models, including S. regelii extract against CCl4-induced hepatocellular damage and S. china polysaccharide against APAP-induced acute liver injury via Nrf2-ARE activation. Astilbin and smilagenin are identified as the principal hepatoprotective compounds. Traditional use for liver diseases is documented across multiple cultures.

• sophoraScientific

  Matrine and oxymatrine from S. flavescens have Chinese regulatory approval for treatment of chronic hepatitis B, with documented hepatoprotective, antifibrotic, and antiviral properties. S. flavescens extract reduces ALT and AST in alcohol-induced liver disease models. The liver is the central organ for Sophora's most clinically substantiated applications.

• soursopScientific

  A. muricata leaf extracts demonstrate hepatoprotective activity against chemically induced liver damage in rodents, reducing liver enzyme elevation and restoring bilirubin to normal levels. Traditional use for liver diseases and jaundice is also well-documented.

• soyScientific

  Soy isoflavones improve liver antioxidant enzyme activity (catalase, total antioxidative capacity) and reduce oxidative markers in animal studies. In human RCTs, soy protein reduces liver-metabolized lipid markers (LDL, total cholesterol, CRP) consistent with hepatoprotective effects. Soy isoflavones also modulate aromatase activity relevant to hepatic estrogen metabolism.

• spearmint leafScientific

  Spearmint extracts and their principal phenolic rosmarinic acid have demonstrated hepatoprotective effects in animal models, reducing liver enzyme elevation (ALT, ALP), oxidative stress, and fibrosis markers. Multiple pharmacological reviews list hepatoprotective activity among M. spicata's established preclinical properties.

• sphaeranthus indicusScientific

  Hepatoprotective activity is one of the most consistently documented pharmacological properties of S. indicus, supported by multiple preclinical studies and listed as scientifically evidenced in major phytopharmacological reviews. Traditional use in Ayurveda for jaundice and hepatopathy further supports this.

• spinachScientific

  Spinach exhibits hepatoprotective activity documented in animal models, with antioxidant phytochemicals reducing hepatic lipid peroxidation and supporting detoxification enzymes. The 2025 comprehensive ScienceDirect review lists hepatoprotective properties among spinach's evidence-based biological activities.

• spirulinaScientific

  Multiple human clinical studies demonstrate that spirulina supplementation reduces elevated liver enzymes (ALT, AST) and improves fatty liver grade in patients with non-alcoholic fatty liver disease (NAFLD). Its hepatoprotective effects are attributed to the antioxidant, anti-inflammatory, and membrane-stabilizing properties of bioactive compounds such as phycocyanin and chlorophyll. Evidence is promising but largely from small pilot studies, and larger randomized controlled trials are still needed.

• squaleneScientific

  The liver is the primary site of squalene biosynthesis and metabolism: dietary squalene is secreted into VLDL/LDL by the liver and circulates to target tissues. Animal studies show squalene supplementation improved hepatic mitochondrial function in aged rats and has hepatoprotective effects against oxidative insults. Conflicting evidence exists on hepatic steatosis in some animal high-fat-diet models.

• steviaScientific

  Animal studies and in vitro evidence demonstrate stevia extracts reduce hepatic steatosis, lower liver enzyme markers (AST, ALT), and protect against chemically induced liver injury through NF-κB inhibition and Nrf2/antioxidant upregulation. In vivo and in vitro studies show stevia ameliorates liver damage. Human-specific liver endpoint clinical trials have not been conducted.

• stigmasterolScientific

  Stigmasterol reduces hepatic fat accumulation, suppresses lipogenic gene expression, modulates bile acid metabolism, and lowers liver enzymes in toxicity models. It alleviates NAFLD/hepatic steatosis in high-fat diet rodents and demonstrates hepatoprotective activity through gut-liver axis modulation.

• sulforaphaneScientific

  The liver is the primary site of sulforaphane's phase II detoxification enzyme induction via Nrf2. SFN reduces hepatic glucose production, improves fatty liver markers, and protects hepatocytes from oxidative and inflammatory injury. Human RCT data confirm hepatic glucose-production reduction and lipid improvements.

• sumaScientific

  Pfaffia paniculata root extract decreased proliferation and increased apoptosis in a murine hepatocarcinogenesis model without affecting cell communication. Ecdysteroids from Pfaffia are described as having hepatoprotective properties in preclinical data. No human liver studies exist.

• sweet flagScientific

  Hepatoprotective activity of A. calamus is confirmed in preclinical studies with biochemical (ALT, AST normalization) and histopathological evidence. Alcohol-induced hepatotoxicity is ameliorated in rat models. Traditional use for liver troubles is documented across Ayurvedic and Unani systems.

• sweet wormwoodScientific

  A. annua extract has shown hepatoprotective effects in acute liver failure animal models, reducing liver enzymes (AST/ALT) and inflammatory cytokines. Traditional use included treatment of jaundice. However, paradoxically, hepatotoxicity has been reported in humans, and sweet wormwood is among implicated supplements in liver injury registries.

• swertiaScientific

  Hepatoprotective activity is the best-established and most extensively studied pharmacological property of Swertia. Multiple peer-reviewed studies demonstrate protection against chemically-induced liver injury and fibrosis. Key compounds amarogentin and swertiamarin protect against CCl4-, paracetamol-, and D-galactosamine-induced hepatotoxicity in rodent models.

• szechuan lovageScientific

  CX has documented hepatoprotective effects in animal models of liver injury, and inhibits hepatic stellate cell activation relevant to liver fibrosis. Research has confirmed significant protective effects against D-galactose-induced liver injury and anti-hepatic fibrosis activity. CX also enters the Liver meridian in TCM and is used for liver qi stagnation.

• tanshinoneScientific

  Tanshinone IIA (TsIIA), a lipid-soluble compound isolated from Salvia miltiorrhiza (Danshen), has substantial preclinical evidence for hepatoprotective effects covering liver fibrosis, NAFLD/NASH, alcoholic liver injury, and cholestasis. A 2019 preclinical meta-analysis (11 animal studies) confirmed that TsIIA significantly reduced fibrosis and improved liver function in rodent models, primarily through inhibition of hepatic stellate cell (HSC) activation, anti-inflammatory, and antioxidant mechanisms. While the traditional use of Danshen for liver disease in Chinese medicine is centuries old, formal human clinical trials for Tanshinone IIA specifically in liver disease remain limited.

• taurineScientific

  The liver is the primary site of taurine synthesis, bile acid conjugation, and taurine-mediated hepatocyte protection. Clinical meta-analyses confirm taurine supplementation significantly reduces AST and ALT. TUDCA, a taurine-derived bile acid, is clinically approved for hepatobiliary disease.

• teaselScientific

  Hepatoprotective activity is explicitly listed among the confirmed pharmacological activities of Dipsacus asper in a comprehensive peer-reviewed review. TCM also classifies teasel root as a liver tonic, and European herbalists used it for jaundice and liver obstruction. No human liver function trials exist.

• terminaliaScientific

  T. chebula has documented hepatoprotective activity in animal studies with mechanistic data from in vitro hepatocyte studies. Its water extract (TCW) reduces serum liver enzymes (AST, ALT, LDH), restores antioxidant defenses, and reduces hepatic inflammatory cytokines in experimental liver injury. Chebulic acid and ellagitannin derivatives are documented hepatoprotectants in rat hepatocyte models.

• tetrahydro iso-alpha acidsScientific

  THIAA and HHIAA inhibited proliferation and viability of human hepatocarcinoma cell lines (HepG2, Hep3B, Huh7) via NF-κB/mTOR pathway inhibition. In diethylnitrosamine-treated rats, THIAA reduced liver tumor numbers. Related iso-alpha acids inhibited hepatic steatosis, inflammation, and fibrosis in NAFLD mouse and human hepatocyte models. THIAA also modulates liver fatty acid oxidation via PPAR pathways.

• tinospora cordifoliaScientific

  T. cordifolia has extensive preclinical hepatoprotective evidence against CCl4, paracetamol, and ethanol-induced liver damage, normalizing SGOT, SGPT, ALT, AST, and bilirubin. A study in chronic alcoholics showed hepatoprotective and anti-stress effects in humans.

• TMG (trimethylglycine)Scientific

  TMG (trimethylglycine/betaine) has a well-characterized biochemical role in hepatic methylation, acting as a methyl donor that facilitates conversion of homocysteine to methionine via the liver-predominant enzyme betaine-homocysteine methyltransferase (BHMT). This mechanism is linked to the maintenance of S-adenosylmethionine (SAM) levels and reduction of oxidative stress in the liver. Human clinical trials in NAFLD/NASH exist, but results are mixed, and overall the evidence base—while genuinely scientific—remains limited by small sample sizes and study-design weaknesses.

• tocotrienolsScientific

  Three separate clinical RCTs establish tocotrienols as hepatoprotective agents in NAFLD, showing reduced liver enzymes, hepatic steatosis, and inflammation. A 1-year RCT in 87 NAFLD adults found significantly higher hepatic normalization rates with mixed tocotrienols. A 24-week δ-tocotrienol RCT confirmed improvements in ALT, AST, hs-CRP, and MDA.

• trans-pterostilbeneScientific

  Pterostilbene reduces hepatic oxidative stress, attenuates NAFLD/steatohepatitis progression, and modulates lipid metabolism genes via Nrf2, AMPK, SIRT1, and PPAR-α pathways in rodent studies. A human NAFLD combination trial (NR + PTE) found reduced hepatic inflammation markers.

• tributyrinScientific

  Tributyrin is hepatoprotective in multiple animal models, reducing liver steatosis, oxidative stress, and inflammation during high-fat diet, ethanol, and diabetic challenges. After absorption from the gut, high butyrate concentrations appear in the portal vein en route to the liver. Animal studies show reduced hepatic triglycerides and partial reversal of liver histopathology.

• trichosanthesScientific

  T. dioica extracts demonstrate hepatoprotective activity in ferrous sulfate-induced liver injury animal models, significantly reducing liver enzyme markers (AST, ALT, ALP) and providing histopathological liver cell protection. T. kirilowii peel polysaccharide protects HepG2 liver cells from oxidative damage in vitro. T. kirilowii has a long history of clinical use for HBV in China, with trichosanthin showing anti-HBV activity.

• triphalaScientific

  Triphala exerts hepatoprotective effects in animal models of paracetamol and chemical-induced liver toxicity, reducing liver enzyme elevation and oxidative damage. It is classified as 'hepatoprotective' in multiple PMC reviews. Lipid-lowering effects across 12 RCTs indirectly support liver metabolic health.

• turmericScientific

  Curcumin, the principal bioactive polyphenol of turmeric (Curcuma longa), has been studied in multiple human randomized controlled trials (RCTs) and several systematic reviews/meta-analyses for liver support, primarily in non-alcoholic fatty liver disease (NAFLD/MASLD). Clinical evidence demonstrates reductions in liver enzymes (ALT, AST, GGT), hepatic steatosis, and fibrosis markers. Evidence quality is rated low-to-moderate by GRADE assessments, and larger high-quality trials are still needed.

• tylophoraScientific

  Hepatoprotective activity of Tylophora indica extracts has been demonstrated in animal models of liver toxicity induced by ethanol and carbon tetrachloride, with significant reductions in serum hepatic enzyme levels. Ethanolic extract was also shown protective against artesunate-induced liver toxicity. The plant is traditionally used for jaundice across northern Karnataka.

• ubiquinolScientific

  CoQ10 has been studied for its hepatoprotective effects, particularly in non-alcoholic fatty liver disease (NAFLD), which is the hepatic manifestation of metabolic syndrome present in ~60% of MetS patients. Mechanisms include PPARα-mediated fatty acid β-oxidation and antioxidant protection against hepatic oxidative stress and lipid peroxidation. RCT evidence in NAFLD shows improvements in liver enzymes and steatosis markers.

• vanadyl sulfateScientific

  Vanadyl sulfate has a dual and dose/context-dependent relationship with the liver: it reduces hepatic glucose output and reverses diabetes-induced oxidative liver damage in diabetic animal models, but increases hepatotoxic markers (ALT, AST, LPO) and reduces antioxidant enzymes in healthy, non-diabetic animals. One human study found evidence of hepatocellular toxicity at supplemental doses.

• vanillaScientific

  Vanillin and vanillic acid have been repeatedly demonstrated to protect the liver against chemical-induced hepatotoxicity in animal models. Studies show normalization of liver enzymes (ALT, AST), restoration of antioxidant defenses (SOD, CAT, GSH), inhibition of lipid peroxidation, reduction of pro-inflammatory cytokines, and prevention of hepatic necrosis. No human liver studies exist.

• vitamin AScientific

  The liver is the primary organ for vitamin A storage (as retinyl esters in hepatic stellate cells) and metabolism. Vitamin A excess (hypervitaminosis A) is a well-documented cause of hepatotoxicity, progressing from hepatic steatosis to fibrosis and cirrhosis at chronic high doses. Normal vitamin A intake is not hepatotoxic; toxicity typically requires prolonged intake >40,000 IU/day.

• vitamin B1Scientific

  The liver is a primary site of thiamine storage and phosphorylation to its active form, and chronic liver disease significantly impairs thiamine metabolism. Up to 80% of chronic alcoholics with liver disease show thiamine deficiency. Reduced thiamine in liver disease contributes to neurological and metabolic complications.

• vitamin B2Scientific

  The liver is the primary site of riboflavin conversion to its active coenzyme forms FAD and FMN, and stores small riboflavin reserves. FAD-dependent cytochrome P-450 flavocoenzymes in the liver participate in drug and toxin metabolism. Riboflavin is actively transported into liver cells and is involved in hepatic redox homeostasis.

• vitamin B3 (niacin)Scientific

  High-dose nicotinic acid (niacin) is well-documented to cause dose-dependent hepatotoxicity, including elevated liver enzymes and, rarely, fulminant hepatic failure at doses exceeding 1000–3000 mg/day, especially with sustained-release formulations. Niacin is also essential for hepatic NAD+ synthesis supporting normal liver metabolism, making it both indispensable at physiological doses and potentially hepatotoxic at pharmacological doses.

• vitamin B5Scientific

  CoA synthesized from pantothenic acid is required by the liver to metabolize drugs, toxins, bile acids, and fatty acids. B complex vitamins including B5 are recognized as necessary for healthy liver function. Pantethine, the B5 derivative, has also been explored in preliminary research for fatty liver disease.

• vitamin B6Scientific

  The liver is the primary site of vitamin B6 metabolism and conversion to the active coenzyme PLP. Liver disease impairs B6 metabolism and causes deficiency; conversely, emerging evidence associates higher vitamin B6 status with lower risk of liver fibrosis.

• vitamin DScientific

  The liver is the primary site of vitamin D's first metabolic activation step (25-hydroxylation), making liver function central to vitamin D status. Vitamin D deficiency is highly prevalent in chronic liver diseases and inversely correlates with disease severity. Clinical and preclinical evidence supports roles for vitamin D in suppressing hepatic fibrosis, inflammation, and steatosis via the vitamin D receptor (VDR) on hepatic stellate cells, though randomized trial data remain limited and heterogeneous.

• vitamin D3Scientific

  The liver is the primary site of vitamin D3's first metabolic activation step, converting it to 25-hydroxyvitamin D3 (25(OH)D3) via hepatic cytochrome P450 enzymes. Vitamin D deficiency is frequently observed across a range of chronic liver diseases, including NAFLD/NASH, cirrhosis, alcoholic liver disease, and viral hepatitis, and is associated with disease severity. Clinical trials of vitamin D3 supplementation in liver disease—particularly NAFLD/NASH—show mixed but promising results, with some RCTs reporting reductions in liver enzyme levels (ALT) and markers of inflammation, while others show no significant histological benefit. The vitamin D receptor (VDR) is expressed in hepatic cells and its signaling is understood to inhibit pro-fibrotic and pro-inflammatory pathways.

• vitamin EScientific

  Vitamin E (α-tocopherol) has well-documented clinical evidence supporting its use in non-alcoholic fatty liver disease (NAFLD) and its more severe form, nonalcoholic steatohepatitis (NASH). As a potent fat-soluble antioxidant, it counters the oxidative stress central to hepatic steatosis and inflammation. Multiple RCTs and systematic reviews confirm it significantly reduces liver enzyme levels (ALT/AST) and improves histological markers of steatosis and inflammation, though its effect on fibrosis remains inconclusive. The American Association for the Study of Liver Diseases (AASLD) has recommended vitamin E 800 IU/day for nondiabetic adults with biopsy-proven NASH.

• wasabiScientific

  Wasabi ITCs—particularly 6-MSITC and its analogues—are potent inducers of hepatic Phase II detoxification enzymes (glutathione S-transferase, HO-1, ALDH2) via Nrf2/Keap1-ARE pathway activation in liver cells. Animal studies show wasabi protects against hepatic lipid deposition in metabolic syndrome models. Wasabi's long-chain ITCs are reportedly more potent than sulforaphane (broccoli) at this mechanism.

• watercressScientific

  PEITC from watercress modulates hepatic phase I and phase II detoxification enzyme systems in both animal models and indirectly in humans through urinary metabolite studies. PMC-indexed research confirms hepatoprotective and detoxification-enhancing effects of watercress and PEITC. Traditional use for liver disorders is also documented across multiple cultures.

• wheat grassScientific

  Animal studies consistently show wheatgrass extract protects against liver enzyme elevations from hepatotoxic substances, with flavonoids and chlorophyll supporting phase II detoxification enzymes. Human evidence is lacking but animal hepatoprotective data are mechanistically grounded. Traditional use as a liver tonic is well-documented.

• whey proteinScientific

  Whey protein has documented protective effects against hepatic steatosis and NAFLD/MASLD through its antioxidant properties (glutathione elevation), reduction of hepatic triglyceride synthesis, and anti-inflammatory actions. A 2025 MDPI review summarized evidence for whey's impact on MASLD-related manifestations. Animal studies show whey reduces hepatic triglycerides, liver enzymes (ALT/AST), lipid peroxidation, and improves hepatic histology.

• xylooligosaccharidesScientific

  XOS has demonstrated hepatoprotective effects through the gut-liver axis: reducing hepatic triglyceride accumulation, lowering liver enzymes (ALT, AST), and ameliorating steatosis in animal models. A 2026 human pilot study in 42 overweight adults (BMI 33.5) tested XOS for four months to validate hepatic steatosis reduction, building on robust animal data.

• yarrowScientific

  Yarrow demonstrates hepatoprotective activity in animal models, reducing toxic liver injury and liver enzyme elevations. Commission E approves it for hepato-biliary disorders. The choleretic, antioxidant, and anti-inflammatory mechanisms collectively support hepatic function.

• yellow rootScientific

  Yellow Root has traditional use for jaundice and liver complaints, and its berberine content has well-documented hepatoprotective effects studied in human clinical trials and meta-analyses. Berberine improves liver enzymes, lipid metabolism, and bile acid regulation in NAFLD and other liver conditions.

• yerba mateScientific

  Animal studies show yerba mate prevents hepatic redox imbalance, reduces liver triglycerides, improves antioxidant enzyme activity, and ameliorates hepatic steatosis. Human crossover trials using AST/ALT markers show no hepatotoxicity and hint at liver protective effects. Dedicated human liver trials are lacking.

• yin chenScientific

  Yin Chen (Artemisia capillaris / A. scoparia) is the most widely used TCM herb for chronic and cholestatic liver disease, with roots in classical texts dating back to the Shennong Bencao Jing. Its key bioactives—scoparone, capillarisin, and chlorogenic acid—demonstrate choleretic, anti-inflammatory, antioxidant, and anti-fibrotic effects in preclinical models. A 2015 meta-analysis of 15 RCTs (1,405 patients) found that the principal Yin Chen formula (Yinchenhao decoction) significantly reduced serum ALT, AST, total bilirubin, and direct bilirubin in cholestasis. Clinical evidence is meaningful but largely derived from Chinese hospital trials and multi-herb formulas, so isolating Yin Chen's independent contribution remains difficult.

• zanthoxylumScientific

  Hepatoprotective effects of Z. armatum are documented in preclinical studies, including attenuation of liver oxidative stress in diabetic and hyperlipidemic animal models. However, Z. armatum also carries documented hepatotoxic risk in high doses via mTOR/ULK1-mediated autophagy suppression and oxidative damage.

• zeaxanthinScientific

  Zeaxanthin dipalmitate (ZD), the predominant form of zeaxanthin in goji berry (Lycium barbarum), has been studied extensively in animal models for hepatoprotective, antifibrotic, and anti-inflammatory effects on the liver. A PMC review confirmed ZD's hepatoprotective, antifibrotic, antioxidant, and anti-inflammatory properties, with its source plant having documented traditional use in Chinese medicine for liver health. Human clinical evidence remains limited; most data derive from preclinical models.

• zeoliteScientific

  Preclinical and indirect clinical evidence supports a hepatoprotective role. In vitro studies show clinoptilolite suppresses inflammatory mediators (NF-κB, TNF-alpha, IL-1B) in liver cells and reverses drug-induced hepatocyte damage. Animal studies demonstrate reduced hepatic heavy metal accumulation. Human clinical evidence is indirect—reduced systemic toxicant load that would otherwise burden the liver—without direct liver function endpoint trials.

• amberTraditional

  In TCM, amber enters the Liver channel, which governs blood and menstruation. Its blood-invigorating action is specifically applied to Liver channel blood stasis presenting as menstrual disorders, abdominal masses, and related conditions. Amber was also historically used for jaundice in European folk medicine.

• apricotTraditional

  Hepatoprotective activity is listed among the primary documented pharmacological properties of Prunus armeniaca in multiple peer-reviewed reviews. Japanese apricot (Prunus mume) extract MK615 has been studied in patients with liver diseases. Traditional medicine systems across Asia use apricot preparations for liver support. Most evidence is preclinical or from the closely related Prunus mume species.

• argan nut oilTraditional

  In LPS-challenged mice, argan oil pretreatment protected against acute liver injury, normalising ALT and AST levels and restoring antioxidant enzyme activities. No human liver function trials exist. Traditional use does not specifically document liver applications.

• ashwagandhaTraditional

  Ashwagandha is listed in Ayurvedic medicine as a liver tonic, and preclinical data suggests hepatoprotective properties. However, paradoxically, pharmacovigilance data document rare but real cases of clinically significant herb-induced liver injury (DILI), documented in peer-reviewed case reports and the NIH LiverTox database.

• asparagusTraditional

  Asparagus has traditional use for liver conditions including jaundice across European, Asian, and Ayurvedic systems. Multiple national pharmacopoeias recognize asparagus for liver/hepatic indications. Animal studies demonstrate hepatoprotective effects against oxidative liver damage from high-cholesterol diets, with upregulation of hepatic antioxidant enzymes.

• assam indigoTraditional

  In TCM theory, Indigo Naturalis (from S. cusia) is described as affecting the liver meridian, and hepatoprotective properties are documented in pharmacological reviews of B. cusia. However, oral Qingdai has also been associated with drug-induced liver injury in clinical use—a double-edged profile.

• bacopaTraditional

  Bacopa monnieri exhibits hepatoprotective activity documented across multiple preclinical models. Animal studies show protection against chemically induced liver damage, restoration of liver enzymes (ALT, AST, ALP), and antioxidant-mediated liver tissue preservation. No human hepatoprotection trials exist.

• birchTraditional

  Birch buds have been used as cholagogues (bile-stimulating agents) in Eastern European and Russian folk medicine, with an associated liver-draining role in gemmotherapy. Birch bark constituents show hepatoprotective activity in preclinical models. A pilot study in chronic hepatitis C patients using birch bark extract reported symptomatic benefit.

• black walnutTraditional

  Traditional Western and Native American herbal practice classifies black walnut as a liver tonic and detoxifying agent. Animal studies show walnut extracts protect against liver toxin-induced damage and high-fat diet hepatotoxicity. No human clinical data for direct liver effects is available.

• blessed thistleTraditional

  Blessed thistle has been used as a liver tonic and hepatoprotective herb in European and Ayurvedic traditions, with applications for jaundice and liver-related sluggishness. Its bitter action stimulates hepatic bile secretion. Animal studies suggest hepatoprotective effects (reduced ALT/AST), but no robust human clinical trials have confirmed liver benefits.

• boswelliaTraditional

  Ayurvedic texts and the Sallai guggal pharmacopoeial reference list Boswellia for liver stimulation and liver disorders. There is no human clinical trial evidence for hepatoprotective effects; animal data are mixed, with some showing hepatotoxicity at high doses.

• bovine liverTraditional

  The traditional 'like supports like' doctrine in many cultural food traditions holds that eating liver supports liver health. Choline from bovine liver is scientifically documented as essential for hepatic fat metabolism; choline deficiency causes non-alcoholic fatty liver disease. Bovine liver is one of the richest dietary sources of choline.

• buckthornTraditional

  Buckthorn has been used in both European and TCM traditional medicine to support liver function, treat jaundice, and act as a liver tonic and blood purifier. TCM assigns it to the Liver meridian with actions including 'tonifying the liver' and 'clearing toxins.' These claims are not supported by clinical evidence and are not recognized by European regulatory monographs.

• calendulaTraditional

  Calendula is traditionally used as a hepatoprotective and cholagogue herb across multiple systems, used for jaundice, liver congestion, and hepatitis. Animal studies confirm hepatoprotective activity. ESCOP lists hepatoprotective activity among in vivo pharmacological findings. No human liver RCTs exist.

• carawayTraditional

  D-carvone, the major component of caraway essential oil, demonstrates hepatoprotective effects in multiple animal studies—reducing liver enzymes, preventing fibrosis, and countering toxin-induced liver damage. Caraway also stimulates bile secretion. Human clinical evidence for liver protection is absent.

• chamomileTraditional

  Chamomile has a traditional history of use for liver disorders documented across multiple cultures. Preclinical studies demonstrate hepatoprotective effects via antioxidant modulation (SOD, glutathione peroxidase) and reduction of AST and ALT by 33–37% in liver-toxicity models. A PMC review identified chamomile as a hepatoprotective plant with modulation of CYP1A2 and anti-inflammatory enzyme activity. Human clinical data are preclinical only.

• champignonTraditional

  Multiple animal studies and in vitro work document hepatoprotective effects of A. bisporus: reduced hepatic steatosis, lower liver enzyme markers (ALT/AST), inhibition of fibrosis progression, and protection against oxidative stress in liver cells. No controlled human clinical trials for liver endpoints have been published, though human RCTs monitoring liver function during supplementation found no adverse effects.

• clerodendrum indicumTraditional

  Hepatoprotective activity is documented as a pharmacological property of the Clerodendrum genus including C. indicum in genus-level reviews. A 2019 study referenced specifically investigated antioxidant-rich active principles of Clerodendrum sp. in haloalkane-induced hepatic damage in a murine model. No dedicated hepatoprotective study on C. indicum specifically has been published.

• cornTraditional

  Corn silk has TCM documentation for liver conditions including jaundice and fatty liver, with preclinical evidence for hepatoprotective activity including attenuation of fatty liver and protection against hepatotoxic agents. Human clinical evidence for liver-specific outcomes is minimal.

• D-glucarateTraditional

  D-Glucarate (as calcium D-glucarate) is widely used to support liver Phase II detoxification via inhibition of beta-glucuronidase, an enzyme that can deconjugate and allow reabsorption of toxins and hormones processed by the liver. The mechanistic rationale is well-characterized in preclinical and in silico research. However, no randomized controlled trials in humans have confirmed clinical benefit for any liver-related indication, so the relationship remains traditionally/empirically used rather than scientifically validated in humans.

• dandelionTraditional

  Dandelion (Taraxacum officinale) has a well-documented traditional role in supporting liver and biliary function, recognized formally by the German Commission E and the EMA as a choleretic agent for bile flow disorders. Preclinical (animal and in vitro) studies consistently show hepatoprotective effects via antioxidant and anti-inflammatory mechanisms, including reductions in ALT/AST and protection against toxic liver injury. However, no robust human clinical trials specifically confirming hepatoprotective efficacy have been published to date, keeping the evidence base firmly in the traditional/preclinical domain.

• elecampaneTraditional

  Elecampane is classified as a liver tonic in traditional Western herbalism and is described as affecting the Liver system in TCM and Ayurveda. Its bitter principles are traditionally held to stimulate hepatic bile production. In vitro data on Nrf2 induction of detoxifying enzymes offers some mechanistic support. No clinical liver studies exist.

• geraniumTraditional

  Geranium has traditional use for liver conditions including jaundice and hepatotoxicity. Preclinical evidence shows hepatoprotective effects via antioxidant mechanisms. Traditional systems including Chinese and African medicine associate geranium with liver health.

• goldenrodTraditional

  Goldenrod has a traditional use for liver conditions, particularly enlargement of the liver, documented in Commission E records and the A.D.A.M. database. Canadian goldenrod is recorded in folk medicine specifically as a liver aid. A 2025 PMC study found hepatoprotective activity of S. canadensis extract in preclinical models. Clinical human evidence is absent.

• guggulTraditional

  Guggul is described as a liver stimulant in Ayurvedic texts and is used for liver detoxification and liver abscess in traditional formulations. Guggulsterones undergo extensive hepatic metabolism and modulate LDL receptor expression and bile acid metabolism. Preclinical studies show hepatoprotective antioxidant effects.

• holarrhena antidysentericaTraditional

  H. antidysenterica is documented in Ayurveda for liver disorders, biliousness, jaundice, and hepatosplenomegaly. Tibetan medicine uses seeds as cholagogue. Preclinical reviews describe hepatoprotective properties via antioxidant mechanisms. No human hepatology clinical studies have been published.

• hollyTraditional

  Fresh I. aquifolium leaf juice is documented in traditional European herbalism for treating jaundice. Preclinical evidence shows I. aquifolium fractions reduce liver adiposity in animal models, offering partial scientific support.

• indian frankincenseTraditional

  Traditional Ayurvedic and Unani texts document Boswellia for liver complaints including jaundice and liver stimulation. Modern pharmacological characterisations note hepatoprotective activity. A clinical trial measuring hepatic enzymes in diabetic patients found Boswellia supplementation had no adverse liver effects. No dedicated hepatoprotection RCT in humans exists.

• indian gum arabic treeTraditional

  Acacia nilotica is traditionally used for liver diseases in Mali and Sudan. Animal studies confirm hepatoprotective effects via antioxidant mechanisms. Gum arabic supplementation in haemodialysis patients reduced liver enzyme markers clinically.

• knotweedTraditional

  Hu Zhang (P. cuspidatum) is listed in the Chinese Pharmacopoeia for removing dampness and reducing jaundice—indicating liver function. It enters the liver meridian in TCM and is traditionally prescribed for hepatitis, liver detoxification, and gallstone conditions. Resveratrol activates Nrf2 and SIRT1 pathways supporting liver detoxification enzyme expression.

• lemonTraditional

  Lemon has a long traditional history of use as a liver tonic and 'detoxifier,' with proposed mechanisms involving bile stimulation and antioxidant protection. While vitamin C's antioxidant role may support hepatocyte protection, no clinical trials confirm a direct detoxifying or hepatoprotective effect specific to lemon.

• lemongrassTraditional

  Lemongrass demonstrates hepatoprotective effects in animal models of drug-induced liver damage. A 2017 study confirmed C. citratus extract protected against paracetamol-induced hepatotoxicity in rats. Antioxidant activity of lemongrass polyphenols provides a plausible hepatoprotective mechanism. Traditional use for liver and detoxification purposes is documented.

• lilacTraditional

  The genus Syringa has extensive traditional use in Chinese medicine for acute icteric hepatitis, and hepatoprotective activity has been confirmed in animal studies for S. vulgaris and related species. S. oblata, a closely related species, has historical clinical use for hepatitis in Chinese hospitals.

• limeTraditional

  Lime is traditionally used as a liver tonic and detoxifying agent in Ayurveda and Southeast Asian medicine. Animal studies demonstrate lime flavonoids (hesperidin, diosmin) reduce hepatic oxidative stress and improve liver function markers. Specific human RCT evidence for lime on liver endpoints is absent.

• neem treeTraditional

  Preclinical studies demonstrate neem extracts protect against CCl4- and paracetamol-induced hepatotoxicity, with nimbolide showing effects comparable to silymarin in animal models. The ScienceDirect overview and multiple PMC reviews list hepatoprotective activity among documented properties. Traditional Ayurvedic use of neem as a liver tonic and blood purifier is extensive. Human clinical trials are absent.

• ox bileTraditional

  Ox bile is bovine-derived bile containing primary bile acids (cholic, chenodeoxycholic, deoxycholic acid) that the liver naturally synthesises. Its relationship to liver support is largely indirect and mechanistic: bile itself is a liver product, and adequate bile flow is integral to hepatic detoxification and cholesterol excretion. However, no clinical trials have directly tested ox bile supplements for improving liver disease outcomes; the clinical evidence base belongs to purified, pharmaceutical-grade bile acids such as UDCA, not OTC ox bile.

• partheniumTraditional

  Liver disease is explicitly documented by the NCCIH as a traditional indication for feverfew across folk and traditional medicine systems. No clinical studies have examined hepatic outcomes. Traditional use is supported only by historical documentation without clinical evidence.

• pennycressTraditional

  T. arvense is classified as a hepatic herb in multiple traditional systems and was used to stimulate bile secretion, support liver function, and cleanse hepatic toxins. Its classification as a depurative and blood purifier in both Chinese and European medicine is closely linked to traditional liver-support concepts.

• plantagoTraditional

  Plantago major extract and P. ovata show hepatoprotective properties in animal models, reducing CCl4-induced and indomethacin-induced liver damage. Antioxidant and anti-inflammatory mechanisms are proposed. Traditional use of P. major for liver conditions is documented in Chinese and European medicine.

• prickly ashTraditional

  Prickly ash is classified as a 'hepatic' in multiple naturopathic herbal monographs, indicating a traditional claim of benefit to liver function. Eclectic medical texts note it 'probably increases hepatic and pancreatic activity.' A preclinical PMC study examined Z. bungeanum constituents for liver oxidative stress attenuation. No human clinical evidence supports a hepatic indication.

• red cloverTraditional

  Red clover has a traditional role in supporting liver function within its 'blood purifier' and 'alterative' herbal classification. Traditional medicine credited it with stimulating bile secretion and liver detoxification. One herbalist monograph notes that its flavonoids have liver-stimulating properties. No clinical trial evidence for hepatic effects has been identified.

• red rootTraditional

  The Naturopathic Herbalist monograph classifies Ceanothus americanus as hepatoprotective and hepatorestorative, with documented traditional use for fatty liver, hepatitis, and jaundice. Clarke's materia medica lists jaundice as a clinical indication. No controlled human hepatic function trials have been published.

• rhodiolaTraditional

  Rhodiola rosea has well-documented hepatoprotective effects in animal and in vitro models, including reductions in hepatic lipid peroxidation, transaminase levels, and lipid droplet accumulation, alongside enhancement of antioxidant enzyme activity. Human clinical evidence for liver protection is absent, placing this in the traditional and pre-clinical category despite mechanistic plausibility.

• rosemaryTraditional

  Rosemary has well-established traditional use as a hepatoprotective and choleretic herb, recognized in folk medicine across multiple cultures. Preclinical studies confirm protection against chemically induced liver damage, and the herb was prescribed for liver conditions by classical physicians including Galen and Hippocrates. Human clinical trial evidence specifically for liver outcomes is lacking.

• sheep's sorrelTraditional

  Sheep's sorrel is classified as a 'depurative' and liver tonic in traditional herbalism, used to support liver function and aid detoxification. Genus-level data show hepatoprotective activity in Rumex species in animal models. No human evidence exists for R. acetosella.

• shepherd's purseTraditional

  Hepatoprotective effects of Capsella bursa-pastoris are documented in preclinical animal studies and consistently listed across pharmacological reviews as an established activity. Traditional use in Russian and Eastern European folk medicine specifically covers liver conditions. Two rat studies by Kuroda (1975, 1976) demonstrated protection against chemically induced hepatocarcinoma.

• siler rootTraditional

  Classical TCM texts state that siler root enters the Liver meridian, and it is used in TCM formulas for harmonizing Liver Qi and relieving Liver-related spasms and constrained Qi. The ScienceDirect polysaccharide review confirms SD 'primarily affects the bladder, spleen, and liver meridians.' No modern clinical or pharmacological studies specifically target liver function with SD.

• snapdragonTraditional

  Traditional use of snapdragon for liver disorders is documented in multiple independent ethnobotanical and pharmacological sources, including Iraqi folk medicine where the whole-plant decoction was used for liver ailments. The use appears in pharmacological reviews as a consistently cited traditional indication. No experimental studies on hepatic effects have been published.

• solomon's sealTraditional

  Solomon's seal is used in European and TCM herbal traditions for liver congestion and fatty liver support. Eclectic physician Fyfe recommended it for 'congestion of the liver.' Modern sources note potential for liver protection, and emodin—a constituent—has documented hepatoprotective activity in vitro.

• stillingiaTraditional

  Stillingia was used in Eclectic and folk medicine for liver affections and congestion, described as a cholagogue and hepatic stimulant. Historical texts document its use for torpid liver, liver congestion, and hepatic disease. No clinical evidence exists.

• thymusTraditional

  Thymol from T. vulgaris has demonstrated hepatoprotective activity in preclinical animal models, reducing liver enzyme elevations (AST, ALT) and histopathological injury markers. The mechanism involves antioxidant protection and modulation of xenobiotic detoxification enzymes. Human clinical evidence is absent; evidence is preclinical.

• tribulusTraditional

  Tribulus is used in Ayurveda and TCM as a hepatoprotective herb, documented across multiple traditional systems. The 2024 phytopharmacology review lists hepatoprotective activity among its traditional indications. Preclinical evidence supports this, though clinical hepatoprotection data are absent.

• wild yamTraditional

  Wild yam is classified as a hepatic herb in multiple herbal traditions, used to relieve hepatic congestion and support liver and gallbladder function. In vitro data show some furostane-type glycosides from D. villosa are hepatoprotective in HepG2 cells. An animal study noted increased liver inflammation with 28-day supplementation at high doses.

• wood betonyTraditional

  Wood betony is traditionally documented as a liver stimulant and tonic, increasing bile discharge and supporting liver function. Historical texts including Gerard list liver conditions as an indication; Russian research cited cholagogue and anti-inflammatory hepatic properties.

• yuccaTraditional

  Liver and gallbladder disorders are listed as traditional oral indications for yucca in clinical reference databases including Drugs.com and Rxlist. Native American traditions used yucca as a body-cleansing agent. Yucca phenolics — particularly resveratrol — have known hepatoprotective properties in the broader literature. No yucca-specific human liver clinical trial exists.