【摘要】 目的 :探讨缺血预处理对急性肾缺血再灌注细胞凋亡及Bcl 2蛋白表达的影响 .方法 :用缺血 8min +再灌 5min预处理在体肾缺血再灌注模型 (n =5 0 ,I4 5min ,I R 6h) ,将动物随机分为 5组 :正常 (A)、假手术 (S)、单纯缺血 (B)、缺血再灌 (C)、预处理 (D) .流式细胞仪检测肾细胞凋亡和细胞增殖周期 ,免疫组化观察Bcl 2蛋白表达 .同时测定血清中BUN ,Cr及MDA含量 .结果 :与正常、假手术组相比 ,缺血再灌注组细胞凋亡率显著增高 (P <0 .0 1) ;与缺血再灌注组相比 ,预处理组细胞凋亡率降低 (P <0 .0 1) ,Bcl 2表达增高(P <0 .0 1) ,细胞增殖指数降低 (P <0 .0 1) ,G0 /G1时段增加(P <0 .0 1) ;与单纯缺血组相比 ,缺血再灌注组细胞凋亡率增高 (P <0 .0 1) ,Bcl 2表达降低 (P <0 .0 5 ) .结论 :细胞凋亡在再灌注期明显升高 ,缺血预处理通过上调Bcl 2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更多还原

【Abstract】 AIM: To investigate the effects of ischemic preconditioning (IPC) on apoptosis, proliferation and Bcl 2 expression known to modulate apoptosis induced by acute renal ischemia/reperfusion. METHODS: Fifty healthy Wistar male rats weighing (250±30) g were anesthetized with 100 mL·L -1 hydratrion chorincalaehyde 0.3 mL and randomly divided into five equal groups with ten animals each. The kidney ischemic preconditioning was induced by circles of left renal ischemia (8 min) separated by reperfusion (5 min) before ischemia reperfusion injury. Right kidneys were removed except group A and ischemia was induced by clamping the left renal pendicle for 45 min by using a nontraumtic vas through a tranverse abdominal incision. The expression of Bcl 2 was observed by immunohistochemistry (SABC) and cell apoptosis and proliferation in the rats were assayed by flow cytometry. RESULTS: The percentage of apoptosis in the I/R group was significantly higher than that in the normal and shame groups ( P <0.01). IPC decreased the percentage of apoptosis and increased A (absorbance) value of bcl 2 protein and the cells of G 0/G 1 phase in the cell cycle as compared with the I/R group. I/R increased the percentage of apoptosis as compared with the ischemia group. CONCLUSION: Apoptosis obviously increases in I/R group and IPC can inhibit the apoptosis induced by renal I/R through upregulating the expression of bcl 2 or modulating the proliferation.更多还原