Ampelopsin, also known as dihydromyricetin (DHM), is a flavonoid compound primarily found in the plant Ampelopsis grossedentata. There is a growing body of scientific research investigating its effects on mitochondrial function. Preclinical studies in cell cultures and animal models suggest that Ampelopsin may support mitochondrial health through several mechanisms. These include enhancing mitochondrial biogenesis, improving mitochondrial membrane potential, and reducing oxidative stress within mitochondria. For example, some studies have shown that Ampelopsin can activate pathways such as AMPK and SIRT1, which are known to promote mitochondrial biogenesis and protect against metabolic stress. Additionally, its antioxidant properties appear to mitigate mitochondrial dysfunction by reducing reactive oxygen species (ROS) production.

Despite this encouraging preclinical evidence, direct clinical trials in humans specifically evaluating Ampelopsin’s effects on mitochondrial health are lacking. Most evidence to date comes from in vitro and animal studies, which, while promising, do not always translate directly to human physiology. Therefore, while there is scientific rationale and early supporting data, the evidence level remains moderate. More robust clinical trials are needed to confirm the efficacy and safety of Ampelopsin for supporting mitochondrial function in humans.