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目的探讨丙泊酚后处理对大鼠肝缺血再灌注损伤的影响。方法成年Wistar大鼠60只,随机分为3组:假手术组(S组,n=12)、缺血再灌注组(IR组,n=12)、丙泊酚后处理组(P组,n=36),丙泊酚后处理分为三个亚组(P1,P2,P4组)。制作70%肝脏缺血再灌注模型,实验结束后即刻取肝左叶做标本。用免疫组化法检测Bcl-2与Bax,TUNEL法检测肝细胞凋亡指数(AI),光镜观察肝组织形态学变化。结果与S组比较,各组Bcl-2、Bax蛋白含量、AI均增加(P<0.01);与IR组比较,P1、P2、P4组Bcl-2蛋白表达增加、Bax蛋白表达和AI减少(P<0.01);与P4组比较,P1、P2组Bcl-2蛋白表达增加、Bax蛋白表达和AI减少(P<0.01)。病理检查显示P1、P2、P4组肝组织结构损伤明显小于IR组。结论丙泊酚后处理可调节Bcl-2、Bax蛋白表达从而减轻肝细胞凋亡,临床剂量丙泊酚对大鼠缺血再灌注肝脏有一定的保护作用。
Objective To investigate the effect of propofol postconditioning on hepatic ischemia-reperfusion injury in rats. Methods Sixty adult Wistar rats were randomly divided into three groups: sham operation group (n = 12), ischemia reperfusion group (n = 12), propofol postconditioning group n = 36). Propofol posttreatment was divided into three subgroups (P1, P2 and P4). 70% hepatic ischemia-reperfusion model was made. After the experiment, the left lobe of the liver was taken as the specimen. Bcl-2 and Bax were detected by immunohistochemistry. Apoptotic index (AI) of hepatocytes was detected by TUNEL method. Morphological changes of liver were observed with light microscope. Results Compared with the S group, the contents of Bcl-2 and Bax protein and AI in each group increased (P <0.01). Compared with the IR group, the expressions of Bcl-2 protein, Bax protein and AI decreased P <0.01). Compared with P4 group, Bcl-2 protein expression and Bax protein expression and AI decreased in P1 and P2 groups (P <0.01). Pathological examination showed that the damage of liver tissue in P1, P2 and P4 groups was significantly less than that in IR group. Conclusion Propofol postconditioning can regulate the expression of Bcl-2 and Bax protein and thus reduce the apoptosis of hepatocytes. The dose of propofol can protect the liver from ischemia-reperfusion in rats.