Fucoidan, a sulfated polysaccharide found mainly in brown seaweeds, has attracted scientific interest for its potential anti-fibrotic properties. Preclinical studies, primarily in cell cultures and animal models, suggest that fucoidan may modulate the processes involved in fibrosis, such as inflammation, oxidative stress, and the deposition of extracellular matrix components like collagen. For instance, research has shown that fucoidan can inhibit the activation of hepatic stellate cells, which are key drivers of liver fibrosis (Wang et al., 2017). Additionally, animal studies report that fucoidan administration reduces markers of fibrosis in lung, kidney, and liver tissues.

The anti-fibrotic effects are thought to be mediated through the suppression of pro-fibrotic cytokines (such as TGF-β1), reduction of oxidative stress, and inhibition of pathways like NF-κB. However, despite these promising findings in laboratory and animal contexts, there is a lack of robust human clinical trials evaluating the efficacy of fucoidan for treating or managing fibrosis in humans. The evidence is thus preliminary and should be interpreted with caution. No major medical guidelines currently recommend fucoidan for fibrosis due to insufficient clinical evidence. In summary, while there is a scientific basis for further investigation, the translation of these findings to human health remains unproven at this time.