Inhibitive effect of cordyceps sinensis on experimental hepatic fibrosis and its possible mechanism.

AIM

To investigate the inhibitive effect and its possible mechanism of Cordyceps Sinensis (CS) on CCl(4)-plus ethanol-induced hepatic fibrogenesis in experimental rats.

METHODS

Rats were randomly allocated into a normal control group, a model control group and a CS group. The latter two groups were administered with CCl(4) and ethanol solution at the beginning of the experiment to induce hepatic fibrosis. The CS group was also treated with CS 10 days after the beginning of CCl(4) and ethanol administration. All control groups were given corresponding placebo at the same time. At the end of the 9th week, rats in each group were humanely sacrificed. Blood and tissue specimens were taken. Biochemical, radioimmunological, immunohistochemical and molecular biological examinations were used to determine the level change of ALT, AST, HA, LN content in serum and TGFbeta(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 dropped in CS group (86.0+/-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 TGFbeta(1) and its mRNA, collagen I mRNA were also markedly decreased (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). More dramatical drop could be seen in PDGF expression (0.87+/-0.43 vs 1.91+/-0.74, P<0.01). Although there was no statistical significance, it was still strongly suggested that collagen III mRNA expression was also decreased in CS group as compared with model control group (0.36+/-0.27 vs 0.95+/-0.65, P=0.0615). In this experiment, no significant change could be found in PDGF mRNA expression between two groups (0.35+/-0.34 vs 0.70+/-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 liver function. Its possible mechanism involves inhibiting TGFbeta(1) expression, and thereby, down regulating PDGF expression, preventing HSC activation and deposition of procollagen I and III.