Effect of compound rhodiola sachalinensis A Bor on CCl4-induced liver fibrosis in rats and its probable molecular mechanisms.

Aim: To explore the anti-fibrotic effect of a traditional Chinese medicine, compound rhodiola sachalinensis A Bor on CCl(4)-induced liver fibrosis in rats and its probable molecular mechanisms.
Methods: Ninety healthy male SD rats were randomly divided into three groups: normal group (n=10), treatment group of compound rhodiola sachalinensis A Bor (n=40) and CCl(4)-induced model group (n=40). The liver fibrosis was induced by CCl(4) subcutaneous injection. Treatment group was administered with compound rhodiola sachalinensis A Bor (0.5 g/kg) once a day at the same time. Then the activities of several serum fibrosis-associated enzymes: alanine aminotransferase (ALT), aspartate aminotransferase (AST), N-acetyl-beta-D-glucosaminidase (beta-NAG) and the levels of serum procollagen III (PCIII), collagen IV (CIV), hyaluronic acid (HA) were assayed. The histopathological changes were observed with HE, VG and Masson stain. The expression of TGF-beta1 mRNA, alpha1 (I) mRNA and Na(+)/Ca(2+) exchanger (NCX) mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR) in situ.
Results: Compound rhodiola sachalinensis A Bor significantly reduced serum activities of ALT, AST, beta-NAG and decreased the levels of PCIII, CIV, HA, improved the liver histopathological changes, inhibited the expression of TGF-beta1 mRNA, alpha (I) mRNA and Na(+)/Ca(2+) exchanger mRNA in rats.
Conclusion: Compound rhodiola sachalinensis A Bor can intervene in CCl(4)-induced liver fibrosis in rats, in which potential mechanisms may be decreasing the production of TGF-beta1, reducing the production of collagen, preventing the activation of hepatic stellate cell (HSC) and inhibiting the expression of TGF-beta1 mRNA, alpha1(I) mRNA and Na(+)/Ca(2+) exchanger mRNA.