| Objective:To further evaluate the effects of valsartan in rats with the expression of the TGFβ1Smad3and Smad7, so as to seek and enrich effective methods for clinical treatment of liver fibrosis.Methods:6wister rats were randomly selected from42wister rats as the normal group, ordinary diet.And the other rats(n=36)were established the liver fibrosis models with the metheds of multiple factors,totally for8weeks.Each6rats in the model group were killed at the2,4,6and8weekend, totally24rats.12rats were randomly allocated into a model control group(n=6) and the valsartan group (n=6). The latter was poured the20mg/kg valsartan into stomach every day after8weeks, the normal control group and model control group were poured the20mg/kg normal saline into stomach, two weeks after all were killed. All rats were determined the content of the TGF β1in serum by Enzyme-linked immunosorbent assay (ELASA).The Smad3and Smad7in liver tissue were assessed by immunohistochemical staining. Histopathological study of liver tissue was done with hematoxylin-eosin (HE) and Masson trichrome staining.Results:(1) Compared with the normal control group,the model rats of the2,4,6,8weekends groups,the content of the TGF β1in serum and the expression of the Smad3in liver tissue progressive increased, and the expression of the Smad7in liver tissue progressive reduced (P<0.01);(2) Two weeks after giving valsartan intervention, the content of the TGF β1in serum and the expression of the Smad3in liver tissue in model groups significantly reduced, at the same period, the expression of the Smad7significantly increased(P<0.01).;(3) Morphological studies showed that there was an increasing degree of hepatic fibrosis in rats of the model group compared with that of the control group, eventually the false flocculus form.Two weeks after giving valsartan intervention,the degree of the liver fibrosis reduced, lobular architecture been restored.Conclusion:Valsartan through liver fibrosis rat can reduced TGF β1/Smad3expression, but also increase Smad7expression, to reduce the activation and proliferation of hepatic stellate cell (HSC), and then reduce ECM, at tne end of playing the role of the antioxidant liver fibrosis. |