Objective： Succinate and succinate receptor (G-protein coupled receptor91, GPR91) signaling pathway has now emerged as a regulator of metabolic signaling. The previous study showed that succinate and its’ specific GPR91 are involved in the activation of hepatic stellate cells(HSCs) and the overexpression of ^-smooth muscle actin (O-SMA). Many studies have shown that metformin not only prevented but also reversed steatosis and inflammation in nonalcoholic steatohepatitis animal model. But the role of metformin in HSCs activation and saccinate-GPR91 signaling is not clarified. Methods： We used LX2 cells, immortalized human stellate cells, as for in vitro study. Male C57BJ6 mice were randomly divided into 3 groups and fed with the methionine- choline-deficient diet (MCD diet group) as a NASH mouse model, or control methionine- choline-sufficient (MCS) diet group and MCD diet + 10% metformin for 12 weeks. Results： In our study, metformin, an insulin sensitizer, and AICAR which is an analog of adenosine monophosphate are proved to suppress the expression of -SMA by enhanced phosphorylation levels of AMPK and inhibition of succinate-GPR91 signaling pathway in palmitate- and succinate-induced LX-2 cells activation. Besides that, metformin and AICAR reduced succinate concentration in cell lysate when LX-2 cells were treated with palmitate. Moreover, metformin and AICAR reduced IL-6, TGF-^1 production in succinate-treated LX-2 cells. Both metformin and AICAR have inhibitory effects on succinate-stimulated HSC proliferation and cell migration. In vivo study, the mice fed MCD diet demonstrated an increase steatohepatitis and liver fibrosis in comparison to the control diet. Metformin administration ameliorated inflammatory cytokine production such as IL-1 and TGF beta-1 in MCD diet fed mice compared with control mice and decreased α-SMA and GPR91 overexpression in the liver of MCD diet- induced NASH model. Conclusion： Metformin has the potential therapeutic for treating steatohepatitis and liver fibrosis.