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

rats were treated with intraperitoneal injection of DMN (5 mg ·kg-1) for three continuous days 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 componentsC12 (800 mg ·kg-1 ·d-1 and 5 mg ·kg-1 ·d-1) for 2 weeks.All the rats were sacrificed to harvest blood and liver tissue sample. Serum alanine aminotransferase(ALT) and aspartate transferase (AST) were detected

maleic dialdehyde (MDA)

superoxide dismutase (SOD)

glutathione peroxidase (GSH-Px) and glutathiones s transferase (GST) in liver tissue were assayed biochemically. Content of hydroxyproline (Hyp) in liver tissue was assayed biochemically;Histological changes with collagen deposition with sirus red staining in rat liver tissue were observed. Expression of α-smooth muscle action (α-SMA)

transforming growth factor-β1 (TGF-β1)

hepatocyte growth factor (HGF-α) and tumor necrosis factor-α (TNF-α) were detected immunohistologically. Result: Compared to 6 wk model group

serum ALT and AST in CsB and C12 group were lowered( P <0.05).Compared to 6 wk model group

Hyp content in liver tissue in CsB and C12 group was decreased significantly ( P <0.05). Large area of hemorrhage and necrosis

swelling of large amount of hepatocytes

widened portal area

inflammatory cells infiltration

increased collagen deposition

and pseudolobule were seen in liver tissue in the model group. Some histological improvement was seen in CsB group and C12 group. Compared to 6 wk model group

CsB and C12 could increase SOD and GSH-Px activity

meanwhile decrease MDA and GST activity ( P <0.01). Compared to 6w model group

expression of α-SMA

TGF-β1 and TNF-α in CsB and C12 was decreased obviously ( P <0.01). Conclusion: CsB and C12 blocks development and formation of liver fibrosis induced by dimethylnitrosamine

through protecting hepatocytes to resist liver injury

decreasing synthesis of collagen

inhibiting oxidative stress. CsB and C12 inhibit KCs activation and release of cytokines

which further inhibits HSCs’ activation

synthesis and secretion of ECM.