磷丙泊酚钠后处理对大鼠肝脏缺血再灌注损伤的保护作用及bcl-2/bax蛋白表达的影响

目的研究磷丙泊酚钠后处理对大鼠肝脏缺血再灌注损伤的保护作用及可能机制。方法 48只Sprague-Dawley大鼠,随机分4组,即假手术组（S组）、对照组（C组）、丙泊酚组（P组）、磷丙泊酚钠组（F组）。每组再根据再灌注2 h或4 h分为2个亚组,分别为S2h、C2h、P2h、F2h亚组和S4h、C4h、P4h、F4h亚组,每个亚组6只大鼠。肝脏缺血1 h后恢复再灌注,S组和C组再灌注开始给予生理盐水静脉泵注,P组给予丙泊酚静脉泵注,F组给予磷丙泊酚钠静脉泵注。于肝脏缺血1 h和再灌注结束后,取血测定血清中谷丙转氨酶（ALT）、谷草转氨酶（AST）,同时取左肝石蜡包埋切片测定B淋巴细胞瘤/白血病-2（bcl-2）蛋白、bcl-2相关X蛋白（bax）含量,苏木精-伊红染色后观察形态学,计数坏死肝细胞比例评价损伤程度。结果 C2h、P2h、F2h和C4h、P4h、F4h亚组血清ALT、AST值,坏死细胞比例和肝组织bcl-2和bax蛋白含量分别高于S2h、S4h亚组（P〈0.05）,P2h、F2h和P4h、F4h亚组ALT、AST值、坏死细胞比例和肝组织bax蛋白含量低于C2h、C4h亚组（P〈0.05）,bcl-2蛋白含量分别高于C2h、C4h亚组（P〈0.05）。结论磷丙泊酚钠对肝脏缺血再灌注损伤有保护作用,其保护机制可能和调控bcl-2、bax蛋白的表达有关。

The Effect of Post-conditioning with Fospropofol Disodium on Hepatic Ischemia-reperfusion and Its Influence on the Expression ofbcl-2/bax Protein in Rats

Objective To investigate the effect of post-conditioning with fospropofol disodium on hepatic ischemia- reperfusion （I/R） and its possible mechanism in rats. Methods Forty-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. Results The activity of ALT and AST, the rate of necrosis cells and the amount ofbcl-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）. Conclusion Fospropofol disodium can alleviate hepatic injury induced by ischemia-reperfusion in rats, in which the bcl-2 and bax protein may play important roles.