ABSTRACT
Aim To observe the effects of cytokine signaling inhibition protein-3(SOCS3) on the liver fibrosis progression and reverse.Methods C57BL/6 mouse model was established by subcutaneous injection of carbon tetrachloride(CCl4).After a successful model of fibrosis, one-month normal diet was given to induce the reverse fibrosis model, while normal mice of the same gender and weight were as control group.Mice were sacrificed at 1, 2, 3, 4, 5, 6, 7, 8 weeks, respectively, then the liver tissue was harvested for the observation of its injury by hematoxylin and eosin(HE) staining.Then Masson staining was applied for the detection of changes in collagen, and the immunohistochemistry(IHC) for the observation of type Ⅰ Collagen(Colla-1), alpha smooth muscle actin(α-SMA), transforming growth factor beta 1(TGF-β1) and SOCS3 protein expression.In vitro formation of fibrosis was induced by TGF-β1 stimulating HSC-T6 cell lines, which was then reversed by MDI medium, with co-incubation of HSC-T6 cells with plasmid in the process of the reverse.Western blot was employed to detect SOCS3, Colla-1, α-SMA, TGF-β1 expression.Results The expression of SOCS3 and TGF-β1 increased in mouse model of fibrosis with the worsening fibrosis process and decreased in the reverse process.Over-expression SOCS3 in the reverse process reduced the development of liver fibrosis;meanwhile, the expression of TGF-β1 was also reduced accordingly.Conclusion SOCS3 may influence the development of the liver fibrosis and its reverse via regulating the expression of TGF-β1.