AIM To investigate the inhibitive effect and its possiblemechanism of Cordyceps Sinensis(CS)on CCl_4-plus ethanol-induced hepatic fibrogenesis in experimental rats.METHODS:Rats were randomly allocated into a normalcontrol group,a model control group and a CS group.Thelatter two groups were administered with CCl_4 and ethanolsolution at the beginning of the experiment to induce hepaticfibrosis.The CS group was also treated with CS 10 daysafter the beginning of CCl_4 and ethanol administration.Allcontrol groups were given corresponding placebo at the sametime.At the end of the 9th week,rats in each group werehumanely sacrificed.Blood and tissue specimens were taken.Biochemical,radioimmunolegical,immunohistochemical andmolecular biological examinations were used to determinethe level change of ALT,AST,HA,LN content in serum andTGFβ_1,PDGF,collagen Ⅰ and Ⅲ expression in tissue at eitherprotein or mRNA level or both of them.RESULTS:As compared with the model control group,serum ALT,AST,HA,and LN content levels were markedlydropped in CS group(86.04±34.4 vs 224.3±178.9,146.7±60.2vs272.6±130.1,202.0±79.3 vs316.5±94.1 and 50.4±3.0vs 59.7±9.8,respectively,P<0.05).Tissue expression ofTGFβ_1 and its mRNA,collagen I mRNA were also markedlydecreased(0.2±0.14 vs 1.73±1.40,1.68±0.47 vs 3.17±1.17,1.10±0.84 vs 2.64±1.40,respectively,P<0.05).Moredramatical drop could be seen in PDGF expression(0.87±0.43vs 1.91±0.74,P<0.01).Although there was no statisticalsignificance,it was still strongly suggested that collagen ⅢmRNA expression was also decreased in CS group ascompared with model control group(0.36±0.27 vs0.95±0.65,P=0.0615).In this experiment,no significant change couldbe found in PDGF mRNA expression between two groups(0.35±0.34 vs0.70±0.46,P>0.05).CONCLUSION:Cordyceps sinensis could inhibit hepaticfibrogenesis derived from chronic liver injury,retard thedevelopment of cirrhosis,and notably ameliorate the liverfunction.Its possible mechanism involves inhibiting TGFβ_1expression,and thereby,down regulating PDGF expression,preventing HSC activation and deposition of procollagen Ⅰand Ⅲ. AIM To investigate the inhibititive effect and its possible mechanism of Cordyceps Sinensis (CS) on CCl 4-plus ethanol-induced hepatic fibrogenesis in experimental rats. METHODS: Rats were randomly assigned into a normal control group, a model control group and a CS group. groups were administered with the CCl_4 and ethanolsolution at the beginning of the experiment to induce hepatic fibrosis. The CS group was also treated with CS 10 daysafter the beginning of CCl_4 and ethanol administration. Allcontrol groups were given corresponding placebo at the same time. At the end of the 9th week, rats in each group werehumanely sacrificed.Blood chemistry and radioimmunolegical, immunohistochemical and molecular biological examinations were used to determine the level change of ALT, AST, HA, LN content in serum and TGFβ_1, PDGF, collagen Ⅰ and Ⅲ expression in tissue at either protein or mRNA level or both of them .RESULTS: As compared with the model control group, serum ALT, AST , HA, and LN content levels were markedly decreased in CS group (86.04 ± 34.4 vs 224.3 ± 178.9, 146.7 ± 60.2 vs 272.6 ± 130.1, 202.0 ± 79.3 vs 316.5 ± 94.1 and 50.4 ± 3.0 vs 59.7 ± 9.8, respectively, P <0.05) .Tissue expression of TGFβ_1 and its mRNA, collagen I mRNA were also markedly established (0.2 ± 0.14 vs 1.73 ± 1.40, 1.68 ± 0.47 vs 3.17 ± 1.17, 1.10 ± 0.84 vs 2.64 ± 1.40, respectively, P <0.05) .Moredramatical It was still statistically strong, that was still strongly suggested that collagen Ⅲ mRNA was was decreased in CS group ascompared with model control group (0.36 ± 0.43 vs 1.91 ± 0.74, P <0.01) 0.27 vs 0.95 ± 0.65, P = 0.0615) .In this experiment, no significant change could be found in the PDGF mRNA expression between two groups (0.35 ± 0.34 vs0.70 ± 0.46, P> 0.05) .CONCLUSION: Cordyceps sinensis could inhibit hepatic fibrogenesis derived from chronic liver injury, retard the development of cirrhosis, and notably ameliorate the liverfunction. It mechanism mechanism i nhibiting TGFβ_1expression, and so, down regulating PDGF expression, preventing HSC activation and deposition of procollagen I and III.