瑞芬太尼对大鼠肝脏缺血再灌注早期细胞凋亡的影响

Effect of remifentanil preconditioning on apoptosis of hepatocytes induced by ischemia-reperfusion injury in rats

目的:观察瑞芬太尼对大鼠肝脏缺血再灌注早期细胞凋亡的影响及其机制。方法:SD大鼠54只分为假手术组(S组),生理盐水对照组(C组),瑞芬太尼预处理组(R组)。缺血均为30 min,瑞芬太尼预处理组为缺血前输注瑞芬太尼30 min,生理盐水对照组以相同的速率及容积输注生理盐水。分别在再灌注1,3,5 h处死6只大鼠,取左肝组织检测细胞凋亡及Bc1-2和Bax表达水平。结果:与S组相比,C组细胞凋亡指数、Bax蛋白表达均增高,而瑞芬太尼预处理减弱了缺血再灌注上述指标的升高(P<0.05);C组Bc1-2蛋白表达减少,瑞芬太尼预处理可增强其在肝组织的表达(P<0.05)。光镜和电镜检查显示瑞芬太尼预处理减轻肝缺血再灌注损伤。结论:瑞芬太尼预处理可以抑制大鼠肝脏缺血再灌注损伤早期细胞凋亡,其机制与上调Bc1-2蛋白表达、下调Bax蛋白表达有关。

Objective：To observe the effect of remifentanil preconditioning on cell apoptosis and Bcl-2 and Bax protein induced by ischemia-reperfusion injury in rat liver tissue. Methods ：Fifty-four male SD rats were randomly divided into 3 groups ：group S,group C and group R. The model of partial liver ischemia/reperfusion（I/R） was used. The reperfusion was performed after 30 min ischemia in the lives. The animals were killed at 1,3,5 h reperfusion and left liver tissues was removed for the expression of Bcl-2 and Bax protein was observed by immunohistochemical technique. Apoptosis index was observed by TUNEL. Examination of structure of liver with light microscope and electron microscope. Results：Apoptosis index and Bax protein in group C increased significantly as compared with that in group S（P〈0.05）. These index in group R were lower in group C（P〈0.05）. Bcl-2 protein in group C decreased as compared with that in group S（P〈0.05）. Bcl-2 protein in group R were higher in group C（P〈0.05）. Light microscope and electron microscope showed that apoptosis of liver tissures was attenuated by remifentanil preconditioning. Conclusion：Preconditioning with remifentanil for 30 minites can reduce cell apoptosis in early stage of reperfusion of rat liver by decreasing Bax and increasing Bcl-2 expressing.