缺血后处理对老年大鼠心肌缺血再灌注损伤的保护作用

doi:10.3969/j.issn.1006-7795.2015.01.025

摘要/Abstract

摘要： 目的观察缺血后处理对老年大鼠心肌细胞凋亡的影响,并探讨细胞凋亡与氧化损伤的关系.方法老年雄性Wistar大鼠90只,采用数字表法随机分成3组(n=30):老年假手术组(saline control, SC组)、老年缺血再灌注组(ischemia/reperfusion,I/R组)和老年缺血后处理组(ischemic postconditioning,IPC 组).制备缺血再灌注损伤和缺血后处理模型,分析检测老年大鼠心肌组织的细胞凋亡情况,测定再灌注末抽血离心测定血清超氧化物歧化酶(superoxide dismutase,SOD)活性及丙二醛(malonaldehyde, MDA)浓度.结果 I/R组心肌细胞凋亡指数平均为53.99±10.54,IPC组平均凋亡指数为45.51±8.81,差异有统计学意义(P<0.01);I/R组血清SOD活性平均为(277.70±29.55)U/mL,IPC组平均质量浓度为(303.72±25.25)U/mL,差异有统计学意义(P<0.05);I/R组血清MDA浓度平均为(25.02±2.35)μmol/L,IPC组平均为(22.54±2.64)μmol/L,差异有统计学意义(P<0.05).结论缺血后处理能够抑制心肌再灌注损伤诱导的细胞凋亡,其机制之一可能与增强心肌细胞抗氧化能力,抑制再灌注所致氧化损伤有关.缺血后处理对老年缺血再灌注心肌具有一定的保护作用.

关键词: 细胞凋亡, 缺血后处理, 缺血再灌注损伤, 老年, 心肌保护

Abstract: Objective To study the effect of ischemic postconditioning(IPC) on cardiomyocyte apoptosis of aged rats with myocardial ischemia reperfusion. Methods The aged(22-24 months) male Wister rats were randomly divided into 3 groups(30 animals in each group): aged sham group, aged ischemic reperfusion group and aged ischemic postconditioning group. Rats in the ischemic reperfusion groups were subjected to 40 minutes of myocardial ischemia by ligating the left anterior descending coronary artery(LAD), followed by a release of the ligature and 6 h of reperfusion. Ischemic postconditionging groups were treated for 40 minutes ischemia, followed by three 10 s cycles of reperfusion and re-occlusion applied at the onset of 6 h of reperfusion. A silk suture around the LAD was not ligated in the sham-operation groups. Myocardial apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL) staining. The levels of superoxide dismutase(SOD) and malonaldehyde(MDA) in serum were detected by colorimetry. Results The aged rat hearts had markedly decreased cardiomyocyte apoptosis in the IPC compared with the IRG[AI(%):45.51±8.81 vs 53.99±10.54, P<0.01]. The serum levels of SOD were higher in the IPC than that in the IRG(277.70±29.55 vs 303.72±25.25, P<0.05), while lower levels of MDA were found in the IPC(25.02±2.35 vs 22.54±2.64, P<0.05). Conclusion The IPC can inhibit cardiomyocyte apoptosis induced by the ischemic reperfusion injury, probably results from the increased antioxidant efficiency while decreased oxidative damage. The IP has protective effects on the acute aged ischemic reperfusion myocardium.

Key words: apoptosis, ischemic postconditioning, myocardial reperfusion injury, aging, cardioprotection

中图分类号:

R743.31

王梦然, 张健, 梁艳红, 陈艳蓉, 李敏, 肖瑶, 宿慧. 缺血后处理对老年大鼠心肌缺血再灌注损伤的保护作用[J]. 首都医科大学学报, 2015, 36(1): 132-136.

Wang Mengran, Zhang Jian, Liang Yanhong, Chen Yanrong, Li Min, Xiao Yao, Xiu Hui. Protective effect of postconditioning on myocardial ischemic reperfusion injury in aged rats[J]. Journal of Capital Medical University, 2015, 36(1): 132-136.

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