Abstract: Objective The purpose of this study was to observe the effect of Mongolian medicine Erligen II on carbon tetrachloride-induced liver fibrosis in rats and explore its possible acting mechanism. Method 58 male SD rats were randomly divided into control, model, low-, moderate- and large-dose of Mongolian medicine Erligen II-intervened groups, and the fibrosis model was established by 40% CCl₄ olive oil solution injection for 8 weeks. Four weeks after modeling, the rats in model group were given intragastrically once daily at different dose of Erligen- II , and in the control group were given the same dose of normal saline for 5 weeks. The pathological changes were observed by HE and Masson staining of liver tissue, and the expression of α-SMA, collagen I and collagen III in liver tissue were detected by immunohistochemistry.Results Serum levels of ALT, AST and HA in moderate dose of Erligen- II-intervened group decreased greatly compared to those in model (P <0.05) , and serum levels of ALT, AST, bilirubin, HA, PIIINP and CIV in large dose of Erligen- II-intervened group decreased significantly compared to those in the model (P<0.05) ; the hepatic expression of α-SMA in control, moderate and large dose of Erligen- II were (0.0±0.0), (4.9±1.0) and (3.4±0.9),significantly weaker than 【(6.1±1.2),P＜0.05】 in model, and that of collagen III were (2.4±1.3), (5.0±2.4) and (3.7±1.8), significantly weaker than 【(6.4±2.4), P＜0.05】 in the model; the hepatic expression of collagen I in the control and in large dose of Erligen- II were (2.1±0.2) and (3.3±1.0), significantly weaker than 【(6.0±2.5), P＜0.05】 in the model; the hepatic fibrosis improved greatly in moderate and large dose Erligen- II groups compared to in the model.Conclusions Mongolian medicine Erligen II has a protective effect on CCl₄-induced liver fibrosis in rats, which might be related to the inhibition of HSC activation and reduction of ECM synthesis.

Key words: Liver fibrosis, Mongolian medicine, Erligen II, α-SMA, Collagen I, Collagen III, Rats