缺血预处理对急性肾缺血再灌注细胞凋亡及ET-1表达的影响

Effect of ischemic preconditioning on apoptosis and expression of ET-1 induced by acute renal ischemia/reperfusion

目的:探讨缺血预处理对急性肾缺血再灌注细胞凋亡及ET-1蛋白表达的影响。方法:采用8 m in缺血+5 m in再灌预处理方式;W istar大鼠分为5组:正常(A)、假手术(S)、缺血(B)、再灌(C)、预处理(D);检测凋亡和细胞增殖周期及肾皮、髓质ET-1蛋白表达。结果:与再灌注组相比,预处理组细胞凋亡率降低(P<0.01),ET-1表达降低(P<0.01),细胞增殖指数降低(P<0.01),G0/G1时段增加(P<0.01)。结论:缺血预处理可通过降低ET-1蛋白的表达和调节细胞增殖周期而抑制肾缺血再灌注细胞凋亡。

Objective：To investigate the effect of ischemic preconditioning （IPC） on renal cell apoptosis, proliferation and expression of ET - 1 induced by acute renal ischemia/reperfusion. Methods： 50 healthy Wistar rats of male weighing 250 ± 30 g were randomly divided into five groups and anesthetized by 10% chloral hydrate at 0.3 ml/100 g body weight. The ischemic preconditioning for kidney was induced before ischemia/reperfusion injury by 4 times of 8 min isehemia plus 5 min reperfusion. The ischemia/reperfusion injury was induced by clamping the left renal pendicle for 45 rain with an atraumatic artery clamp and then 6 hours of reperfusion. The expression of ET -1 was examined by radioimmunology methods. The renal cell apoptosis and proliferation were assayed by flow cytometry. Results： The percentage of cell apoptosis and the expression of ET - 1 in renal cortex and medulla in I/ R groups were significantly higher than those in the normal and sham groups. IPC reduced the percentage of cell apoptosis and index of cell proliferation as well as ET - 1 expression level, but increased the amount of cells in G0/ G1 period. Conclusion： IPC alleviates I/R injury by reducing the expression of ET - 1 and inhibiting cell apoptosis as well as regulating cell cycle.