experimental study on hepatocyte apoptosis induced by acute biliary tract infection

ObjectiveTo examine the occurrence and possible mechanism of hepatocyte apoptosis in acute biliary tract infection. MethodsAfter adaptive feeding for seven days, 30 male rats were randomly divided into five groups (n=6 each), i.e., one control group injected with 0.2 ml of saline through the common bile duct and four experimental groups injected with an equal volume of Escherichia coli cell suspension to build an acute biliary tract infection model. Animals of the control group were killed 6 h after injection of saline, and those of the four experimental groups were killed respectively at the time points of 6, 12, 24, and 48 h after injection of E. coli. Liver tissue specimens were taken from all the rats to prepare tissue sections. Pathological features were examined by hematoxylin-eosin staining and light microscopy. Hepatocyte apoptosis was examined by cell counting after TUNEL staining and calculation of the apoptotic index. The expression of apoptosis-related proteins (Bcl-2 and Bax) was measured by immunohistochemistry. Data comparison between groups was performed by analysis of variance, and pairwise comparisons were further conducted using the LSD-t test and Dunnett′s T3 test. ResultsTissue specimens of the control groups had no significant pathological changes, while those of the experimental groups showed hepatocyte apoptosis. Compared with the control group, the four experimental groups had significantly greater values of apoptotic index (P＜0.05). Additionally, the values of apoptotic index in the 24 and 48 h experimental groups significantly increased over time compared with that of the 12 h experimental group (P＜0.05). Bax protein expression level significantly differed between the control group and the experimental groups (P＜005), showing a slight increasing trend over time in the latter four groups (P＞0.05). Bcl-2 protein expression level had no significant differences between the control group and the 6 or 12 h experimental groups (P＞0.05). Over time, however, significant differences were observed in Bcl-2 expression level between the 12 h experimental group and the 24 or 48 h experimental group (P＜005). ConclusionHepatocyte apoptosis occurs within a short time after acute biliary tract infection. It persists in the whole process of the infection, with increased expression of Bax (inducer of apoptosis) and decreased expression of Bcl-2 (inhibitor of apoptosis). The changes in the expression of apoptosis-related genes coincide with hepatocyte apoptosis, suggesting that hepatocyte apoptosis may be associated with Bax and Bcl-2 genes.