Oxymatrine Attenuates Lipid Accumulation In Hepg2 Cells By Inducing Autophagy

Recent reports have revealed that Oxymatrine (OMT) can alleviate hepatosteatosis. The aim of this study was to explore the underlying molecular mechanisms of OMT in improving lipid accumulation in liver cells, and evaluate the impact of OMT on lipogenesis and autophagy in HepG2 cells exposed to fructose. The effects of OMT on hepatic steatosis were observed by oil red O staining and content detection of triglycerides (TG). The effects of OMT on autophagy were evaluated by MDC staining and an autophagy detection kit. Protein expression levels were examined by Western blot. After 48-hours of intervention with fructose, the TG content was significantly increased compared with the control group. Red staining areas by oil red O staining were increased significantly in the fructose group compared with the control group. After OMT intervention, lipid accumulation was decreased. Results of MDC staining and autophagy detection showed that OMT induced autophagy. Compared with the control group, the expression levels of LC3B, Beclin-1, and Atg7 were significantly decreased, and the expression levels of FAS, SCD1, p-Akt/Akt, and mTOR were increased in the fructose group. Compared with the fructose group, expression levels of FAS, SCD1, p-Akt/Akt, and mTOR were decreased, and the expression levels of LC3B, Beclin-1, and Atg7 were significantly increased in the OMT group. Inhibition of autophagy by beclin-1 siRNA increased expression of srebp-1, Fas, p-Akt/Akt, and mTOR, and expression of LC3B, Beclin-1, and Atg7 was decreased. OMT can thus inhibit lipid accumulation of HepG2 cells by activating autophagy through the Akt-mTOR signaling pathway.