延迟预适应减少大鼠心肌缺血再灌注的细胞凋亡

基础医学与临床 ›› 2009, Vol. 29 ›› Issue (4): 379-382.

延迟预适应减少大鼠心肌缺血再灌注的细胞凋亡

刘颖聂咏梅吴伟康

广东药学院

收稿日期:2008-06-30 修回日期:2008-09-10 出版日期:2009-04-25 发布日期:2009-04-25
通讯作者: 刘颖

Delayed preconditioning reduced apoptosis of myocardial cells in rats

Ying LIU, Yong-mei NIE, Wei-kang WU

Guangdong Pharmacological College

Received:2008-06-30 Revised:2008-09-10 Online:2009-04-25 Published:2009-04-25
Contact: Ying LIU,

摘要/Abstract

摘要： 目的以SMAC和XIAP的表达变化为着眼点，探讨心肌缺血延迟预适应抗心缺血再灌注（MI/R）后细胞凋亡的机制。方法 SD大鼠分为对照组、假手术组、缺血再灌注组、延迟缺血预处理组。缺血再灌注组采用经典大鼠冠脉结扎，缺血1h，再灌1h。延迟缺血预处理组采用缺血5 min，再灌5 min，反复循环3次，24 h后缺血1 h，再灌1 h。流式细胞仪测定心肌细胞凋亡率，检测caspase-3活性，Western blot分析胞质SMAC及XIAP的表达。结果与对照组相比，缺血再灌注组细胞凋亡率、caspase-3的活性及SMAC的表达明显升高（P<0.01），XIAP的表达明显下降（P <0.01）。延迟缺血预处理组细胞凋亡率、caspase-3的活性及SMAC的表达较缺血再灌注组明显下降（P<0.01），XIAP的表达较缺血再灌注组升高（P <0.01）。结论心肌缺血延迟预适应可以减少MI/R造成的细胞凋亡，机制与其阻碍SMAC自线粒体释放，从而保护XIAP对caspase家族的抑制密切相关。

关键词: 缺血再灌注损伤, 延迟预适应, Smac, XIAP

Abstract: Objective Investigate the relation between decrease of apoptosis caused by delayed preconditioning and expression of SMAC and XIAP. Methods Sprage－Dawleyt rats were divided into four groups: control, sham, I/R and IPC/SWOP. The rats in I/R group underwent ischemia for 1 hour by classic artery ligation and reperfusion for 1 hour. The rats in IPC/SWOP group underwent tree cycles of 5-minute ischemia and 5-minute reperfusion 24 hours prior to the index occlusion. Cell apoptosis was measured by flow cytometry, the activity of caspase-3 was also measured. The expression of SMAC and XIAP in cytosol of myocardial cell was analyzed by Western blot. Results Cell apoptosis rate, activity of caspase-3 and expression of SMAC increased significantly in I/R compared with control (p<0.01). The expression of XIAP decreased in I/R compared with control (p<0.01). In IPC/SWOP, cell apoptosis rate, activity of caspase-3 and expression of SMAC decreased significantly compared with I/R (p<0.01). The expression of XIAP increased in IPC/SWOP compared with I/R (p<0.01). Conclusion Myocardial ischemia delayed preconditioning can suppress apoptosis caused by MI/R, the mechanism is related to inhibition of SMAC release from Mitochondria, and in turn maintaining the inhibition of caspase family by XIAP.

Key words: ischemia-reperfusion injury, delayed preconditioning, Smac, XIAP

刘颖聂咏梅吴伟康. 延迟预适应减少大鼠心肌缺血再灌注的细胞凋亡[J]. 基础医学与临床, 2009, 29(4): 379-382.

Ying LIU; Yong-mei NIE; Wei-kang WU. Delayed preconditioning reduced apoptosis of myocardial cells in rats[J]. Basic & Clinical Medicine, 2009, 29(4): 379-382.

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