“This study delves into the mechanism of action of gastrodin in the treatment of non-alcoholic fatty liver disease (NAFLD), injecting new vitality into the research in this field. Researchers used a high-fat and high cholesterol diet (HFHC) induced mouse model and a Huh7 cell model to simulate the pathological environment of NAFLD, and observed the effects of gastrodin on lipid metabolism in mice and cell models. Research has found that gastrodin can significantly reduce the levels of total cholesterol, low-density lipoprotein cholesterol, and triglycerides in mouse serum, significantly improve fatty liver disease, and reduce lipid content in the liver. Meanwhile, in vitro experiments showed that gastrodin significantly reduced the lipid accumulation level in Huh7 cells. These results all indicate that gastrodin has significant effects in reducing hepatic lipid accumulation and blood lipid levels. Further mechanistic studies suggest that the action of gastrodin may be related to regulating the steroid regulatory element binding protein 1c (SREBP1c) signaling pathway. This pathway plays a crucial role in lipid synthesis, and gastrodin can significantly reduce the expression levels of SREBP1c and its downstream lipid synthesis related genes in mice and Huh7 cells, thereby inhibiting lipid synthesis. This discovery provides a new perspective for understanding the mechanism of action of gastrodin in treating NAFLD. In summary, the results of this study reveal the potential of gastrodin in reducing hepatic lipid accumulation and lipid levels, improving NAFLD, and preliminarily elucidating its mechanism of action. This discovery provides new candidate drugs and research directions for the treatment of NAFLD, which is expected to bring new breakthroughs to the development of this field.”