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

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8min缺血＋5min再灌预处理方式；Wistar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。

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

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.