| Aim: to investigate the effects and mechanisms of Yuegan capsule on liverfibrosis induced by dimethylnitrosamine (DMN). Methods: the animal modelswere made with 0.5% DMN ip. 3 days every week for 4 weeks. During the time, Yuegan capsule was administrated at the dose of 2.5mg/kg, 5mg/kg or 10mg/kg once a day compared with recombinant human interferon α -2a for injection. We detected and measured the content of hydroxyproline in liver homogenate, and observed the expression of alpha-smooth muscle actin (a-SMA), matrix metalloproteinase-1 (MMP1) and the tissue inhibitor of metalloproteinase-1 (TIMP-1) by immunohistochemical method. The liver pathological changes and the deposition of collagen were observed with HE staining and Sirius red staining.Results: The level of hydroxyproline in normal liver was 0.246 ± 0.056μg / mgprot. In the model group, hydroxyproline levels were significantly increased (0.682±0.039μg/mgprot, P<0.05). in the middle dose group (0.448±0.050 μg / mg prot), high dose group(0.419±0.048μg/mgprot) and recombinant human interferon a-2a control group(0.298±0.033μg/mgprot), the hydroxyproline levels were lower than the model group(P<0.05). the deposition of collagen in the middle dose group ,high dose group and recombinant human interferon a-2a control group was also palliiative compared with the model group. The fibrosis evolution was inhibited. Alpha-smooth muscle actin (a-SMA) and the tissue inhibitor of metalloproteinase-1 (TIMP-1) in model group were intensive compared with the normal group in which a-SMA and TIMP-1 had almost no expression. The expressions of them in other groups were light compared with the model group(p<0.05). MMP-1 in all groups were slight and have no distinct discrepancy.Conclusions: Yuegan capsule is effective in protecting against DMN-inducedliver fibrosis in rats. The mechanisms of the protection may due to inhibit the activity of hepatic stellate cell (HSC), then reduce the synthesis of the collagen and promote its degradation.
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