ObjectiveTo investigate the effect of post-conditioning with fospropofol disodium on hepatic ischemiareperfusion (I/R) and its possible mechanism in rats. MethodsForty-eight Sprague-Dawley rats were randomly divided into four groups, including sham group (S), control group (C), propofol group (P) and fospropofol disodium group (F). According to the different periods after reperfusion, each group was further divided into 2-hour and 4-hour reperfusion subgroups respectively (n=6 in each subgroup), named S2h, C2h, P2h, and F2h subgroups and S4h, C4h, P4h, and F4h subgroups. The livers of rats were reperfused after hepatic ischemia for one hour. In the beginning of reperfusion, normal saline was infused intravenously in group S and group C continuously, propofol was infused intravenously in group P continuously, fospropofol disodium was infused continuously in group F. The blood was sampled at the end of ischemia and reperfusion for assay of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The bcl-2 and bax protein contents in liver tissue were detected by immunohistochemical analysis, and liver samples were stained with hematoxylin-eosine for histological observation and damage degree evaluation by counting the proportion of necrosis cells. ResultsThe activity of ALT and AST, the rate of necrosis cells and the amount of bcl-2 and bax protein after reperfusion in group C, group P and group F were higher than those in group S at matched reperfusion time points (P<0.05). The activity of ALT and AST, the proportion of necrosis cells and bax protein contents decreased in group P and group F, compared with group C at the same reperfusion time points, while the contents of bcl-2 protein were significantly increased (P<0.05). ConclusionFospropofol disodium can alleviate hepatic injury induced by ischemia-reperfusion in rats, in which the bcl-2 and bax protein may play important roles.