Apigenin reduces the excessive accumulation of lipids induced by palmitic acid via the AMPK signaling pathway in HepG2 cells.

In recent years, increasing attention has been paid to diseases caused by excessive accumulation of lipids in the liver with therapeutic agents derived from natural products offering an alternative treatment to conventional therapies. Among these therapeutic agents, apigenin, a natural flavonoid, has been proven to exert various beneficial biological effects. In the present study, the antiadipogenic effects of apigenin in HepG2 cells was investigated. It was demonstrated that the treatment of cells with different concentrations of apigenin for 24 h significantly decreased the palmitic acid-induced increases in total cholesterol (TC) and triglyceride (TG) levels as well as intracellular lipid accumulation. In addition, apigenin increased the phosphorylated-AMP-activated protein kinase (AMPK) levels but decreased the expression levels of 3-hydroxy-3-methylglutaryl CoA reductase, sterol regulatory element-binding protein (SREBP)-1, fatty acid synthase, and SREBP-2 in a concentration-dependent manner. The present findings suggested that apigenin might improve lipid metabolism by activating the AMPK/SREBP pathway to reduce lipid accumulation in the liver.