Effects Of The Huo-Xue-Shen-Shi-Fang On Expression Of Fas, FasL, Bcl-2 And Bax In Liver Tissue Of Rats With Hepatic Fibrosis

Objective To observe the expression of Fas , FasL ,Bcl-2 and Bax in rat hepatic fibrosis model and study the possible mechanisms of treating hepatic fibrosis of Huo-Xue-Shen-Shi-Fang (HXSSF) by observing the function of HXSSF on the expression of these proteins in rat hepatic fibrosis model.Methods Hepatic fibrosis was successfully induced in rats by subcutaneous injection of 40% carbon tetrachloride (CC14), the rats were divided into fibrosis model group, HXSSF treatment group and Fu-Fang-Bie-Jia-Ruan-Gan-Tablet positive control group, normal control group was another group of 20 normal rats. After 12-week-treatment, serum hyaluronic acid was examined, histopathological changes and degrees of fibrosis were observed by optical microscopy. Meanwhile, the expression of Fas,FasL,Bcl-2 and Bax proteins was detected by immunohistochemistry and quantified by using computerized image analysis.Results It was found that the serum hyaluronic acid index and degrees of fibrosis of HXSSF treatment group was significantly decreased and lower than the fibrosis model group (P<0.05) , but there was no noticeable difference between the HXSSF treatment group and the positive control group (P>0.05). Compared with that in normal control group ,the expression of Bcl-2, Bax, Fas and FasL was significantly increased in rat fibrosis model(P <0.01). There was no noticeable difference in expression of Fas and fasL between the HXSSFtreatment group and the fibrosis model group (P>0.05). Compared with that in fibrosis model, the expression of Bcl-2 was significantly lower in fibrous septae of the rats treated with HXSSF(P <0.05), and the expression of Bax was not significantly different in fibrous septae(P >0.05). So the proportion of Bax/Bcl-2 was significantly increased in fibrous septae(P<0.05).Conclusion HXSSF has significant results on treating experimental hepatic fibrosis. The expression of Fas and FasL proteins have increased in liver tissue with experimental hepatic fibrosis. FasL proteins only expressed in fibrous septae of the rats with hepatic fibrosis. Fas system induced the apoptosis of cells in fibrous septae. HXSSF has no signifcant effect on the expression of Fas and FasL in hepatic fibrosis model rats. The expression of Bcl-2 and Bax proteins have increased in liver tissue with experimental hepatic fibrosis. After being treated by HXSSF, the proportion of Bax to Bcl-2 was significantly increased in fibrous septae of the rats with hepatic fibrosis. HXSSF could promote the apoptosis of cells in fibrous septae. Promoting myofibroblast cells apoptosis was possibly one of the mechanisms of HXSSF treating hepatic fibrosis.