Improving Effect of Total Flavone from Litchi chinensis on the Hepatocyte Injury in Liver Fibrosis Model Rats / 中国药房

ABSTRACT

OBJECTIVE:To study the improving effect of total flavone from Litchi chinensis (TFL) on the hepatocyte injury in rats with liver fibrosis. METHODS:The rats were given dimethylnitrosamine(DMN),ip,once a day in the first 3 d of every week,which lasted for 30 consecutive days to establish hepatocyte injury model. 60 rats were equally randomized into a normal control(isometric normal saline)group,a model(isometric normal saline)group and the groups of high and low-dose TFL(200 and 100 mg/kg). When the model was being established,drugs were administered,ig,once a day for 45 consecutive days except for normal control group. HE staining was performed,and then the rats’hepatocytes were observed under the microscope and path-ological stage (S1-S4) of liver tissue was analyzed. Masson staining and immunohistochemical staining were conducted,and then the rats’hepatocytes were observed under the microscope and calculation was made for the degree of liver fibrosis and the expres-sion of Bcl-2 and Bax. The activities of aspartate aminotransferase(AST)and alanine aminotransferase(ALT)in rats’serum were determined. RESULTS:The pathological stages of liver cell of rats in the model group were mainly stages S3 and S4 and the groups of high and low doses TFL were dominated by stages S1 and S2. Compared to the rats in the normal control group,those in the mod-el group had higher degree of liver fibrosis,expression of Bcl-2 and Bax and activities of AST and ALT in serum. Compared to the rats in the model group,those in the groups of high and low doses TFL had lower degree of liver fibrosis,higher expression of Bcl-2,lower expression of Bax,and lower activities of AST and ALT in serum. There were statistically significance (P<0.05). CONCLUSIONS:TFL can alleviate the hepatocyte injury in rats with liver fibrosis to some degree by a mechanism which may be related to the up-regulation the expression of Bcl-2 and the down-regulation of the expression of Bax.