Objective: To study the effect and mechanism of CsB and its effective components on liver fibrosis in rats induced by dimethylnitrosamine (DMN). Method: From the 1st to 4th week

rats were treated with intraperitoneal injection of DMN (5 mg·kg-1) for three continuous day each week. After modeling

normal group and model group were given saline (10 mL·kg-1) intragastrically

and rats in drug treatment group were treated separately with CsB and its components C12 (800 mg·kg-1·d-1 and 5 mg·kg-1·d-1) for 2 weeks. After all courses of treatment

all rats were sacrificed to harvest blood and liver tissue sample.Serum alanine aminotransferase(ALT)

aspartate transferase (AST)

albumin (Alb)

total bilirubin (TBil) and content of hydroxyproline (Hyp)in liver tissue were detected. Histological changes with HE staining and collagen deposition with sirus red staining in rat liver tissue were observed. Expression of hepatocyte growth factor (HGF-α) and tumor necrosis factor-α (TNF-α) were detected immunohistologically. Result: Compared with 6 weeks model group

serum ALT and AST activity

TBil content and Hyp content in liver tissue in CsB and C12 group lowered and Alb content increased significantly (P<0.05). Compared with 6 weeks model group

some histological improvement was made in CsB and C12 group. Compared with the 6 wk model group

HGF-α protein expression in liver tissue in CsB and C12 group increased significantly(P<0.01). Compared with 6 weeks model group

quantity apoptotic hepatocytes in Cs and C12 group decreased obviously (P<0.01). Conclusion: CsB and C12 can block development and formation of liver fibrosis induced by dimethylnitrosamine

by protecting hepatocytes to resist liver injury

decreasing synthesis of collagen

inhibiting oxidative stress. CsB and C12 can improve the level of expression of HGF-α and inhibit hepatocytes apoptosis to balance apoptosis and proliferation

so as to block or reverse development liver fibrosis.