OBJECTIVETo investigate the dynamic expression of TGF-beta1/Smad protein in rats with liver fibrosis induced by carbon tetrachloride (CCl4), to study mechanism of TGF-beta1/Smad signaling and the relationship between its transduction and liver fibrosis.

METHODSFifty healthy male SD rats were randomly divided into two groups: normal control group and model group. Experimental liver fibrosis was induced by subcutaneous injection of CCl4. After six weeks and nine weeks, histopathological changes and degrees of fibrosis were observed by optical microscopy. Meanwhile, the expression of TGF-beta1, TP3R-I, Smad2/3 and Smad7 proteins was detected by immunohistochemistry.

RESULTS(1) Pathological observation of hepatic specimens: hepatic tissue of model group rat had inflammation and fibrosis in different degrees. By comparing with the degrees of inflammation and fibrosis model groups were more severe than normal control group (P < 0.05). (2) Changes of protein levels about TGF-beta1/Smad: the expressions of TGF-beta1, TbetaR-I, Smad2/3 and Smad7 in rat hepatic tissue were detected with immunohistochemistry techniques. The expressions of the four items in model group were higher than those of normal control group (P < 0.01). In fibrosis model group, there exist considerable positive correlations among expressions of TGF-beta1, TbetaR-I, Smad2/3, Smad7 and degrees of fibrosis in livers (P < 0.05 or 0.01).

CONCLUSIONThere is close relation between the level of TGF-beta1, TbetaR-I, Smad2/3, Smad7 and the different liver fibrosis grades due to CCl4. The up regulation of TGF-beta1, TbetaR- I, Smad2/3 and Smad7 in liver tissue is involved in the progression of hepatic fibrosis.