摘要
目的 :观察缺血预处理 (IPC)对大鼠急性肾缺血 /再灌注损伤的保护作用及其对细胞凋亡及凋亡相关蛋白Bcl 2和Bax表达的影响 ,探讨其作用的可能机制 .方法 :双肾动脉缺血 4 5min再灌注 2 4h制备成急性肾缺血 /再灌注动物模型 ,5 0只Wister大鼠随机分为对照假手术组、缺血 /再灌注组、缺血预处理组 (IPC1 ,IPC2 ,IPC3) .原位末端标记法检测细胞凋亡指数 ,免疫组化法测定Bcl 2和Bax表达 .结果 :与对照组比较 ,缺血 /再灌注组凋亡指数增加 (3.1± 2 .3vs 2 8.8± 4 .4 ,P <0 .0 5 ) ,Bax(1 83.0± 1 2 .8vs1 6 3.0± 1 7.1 ,P <0 .0 5 )表达明显增强 ,Bcl 2增加 (1 84 .0± 9.6vs 1 79.0± 1 3.0 ,P <0 .0 5 ) ,Bcl 2 /Bax比值明显降低 (1 .0 0± 0 .0 8vs 1 .1 0± 0 .0 7,P <0 .0 5 ) .缺血 /再灌注组比较 ,IPC3组肾小管凋亡指数明显下降(2 8.8± 4 .4vs 1 5 .6± 3.8,P <0 .0 5 ) ,Bcl 2表达增强 (1 79.0±1 3.0vs1 70 .0± 1 5 .1 ,P <0 .0 5 ) ,Bax表达减弱 (1 6 3.0± 1 7.1vs1 74 .0± 1 3.7,P <0 .0 5 ) ,Bcl 2 /Bax比值增高 (1 .1 0± 0 .0 7vs0 .98± 0 .1 1 ,P <0 .0 5 ) .结论 :缺血预处理 (IPC3)具有抗肾脏缺血 /再灌注损伤作用 ,其作用机制可能是通过调控Bcl 2 /Bax介导的肾脏缺血
AIM: To investigate the protective effect of ischemic preconditioning (IPC) on rats with acute renal ischemia/reperfusion (I/R) injury, and its effects on cell apoptosis and expression of Bcl 2 and Bax in the cells, and the possible mechanism of renal protection affected by IPC against I/R injury. METHODS: Fifty Wister rats of either sex were randomly divided into 5 groups: Group A (control group) in which sham operation was performed; group B (I/R group), in which ischemia was made by tying both renal arteries for 45 min, followed by 24 hour reperfusion; group C (IPC1 group) in which both renal arteries were first tied for 10 min then untied for 10 min, then followed the procedures as in group B; group D (IPC2 group) in which both renal arteries were first tied for 10 min then untied for 10 min and the process was repeated 2 times before the procedures in group B; group E (IPC3 group) in which both renal arteries were first tied for 10 min then untied for 10 min and the process was repeated 3 times before the procedures in group B. Apoptosis was examined by means of terminal deoxynucleotidyl transferase mediated d UTP nick end labeling (TUNEL). The expression of Bcl 2 and Bax protein was measured by immunohistochemical technique. RESULTS: Compared with those in the control group, the apoptotic index (3.1±2.3 vs 28.8±4.4, P < 0.05) and the expression of Bax (183.0±12.8 vs 163.0± 17.1 , P <0.05) and Bcl 2 (184.0±9.6 vs 179.0±13.0, P < 0.05)were higher, and the Bcl 2/Bax ratio decreased significantly(1.00±0.08 vs 1.10±0.07, P <0.05)in I/R group. Compared with those in the I/R group, the apoptotic index (28.8±4.4 vs 15.6±3.8, P <0.05) and the levels of expression of Bax decreased(163.0±17.1 vs 174.0±13.7, P <0.05), and the expression of Bcl 2 (179.0±13.0 vs 170.0±15.1, P <0.05) and the Bcl 2/Bax ratio increased (1.10±0.07 vs 0.98±0.11, P <0.05)in IPC3 group. CONCLUSION: IPC3 can protect kidneys from I/R injury, partly through the inhibition of apoptosis by regulating Bcl 2 and Bax expression.
出处
《第四军医大学学报》
北大核心
2004年第9期818-821,共4页
Journal of the Fourth Military Medical University
基金
陕西省教育厅 2 0 0 2年科研计划基金 (0 2JK1 88)
