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缺血后处理对 IR 大鼠缺血再灌注诱导的心肌氧化损伤的保护作用。

Protective effect of ischemic postconditioning against ischemia reperfusion-induced myocardium oxidative injury in IR rats.

机构信息

Department of Cardiology, Fengxian Branch of Shanghai 6th People's Hospital, Shanghai, China.

出版信息

Molecules. 2012 Mar 27;17(4):3805-17. doi: 10.3390/molecules17043805.

Abstract

Brief episodes of myocardial ischemia-reperfusion (IR) employed during reperfusion after a prolonged ischemic insult may attenuate the total ischemia-reperfusion injury. This phenomenon has been termed ischemic postconditioning. In the present study, we studied the possible effect of ischemic postconditioning on an ischemic reperfusion (IR)-induced myocardium oxidative injury in rat model. Results showed that ischemic postconditioning could improve arrhythmia cordis, reduce myocardium infarction and serum creatin kinase (CK), lactate dehydrogenase (LDH) and aspartate transaminase (AST) activities in IR rats. In addition, ischemic postconditioning could still decrease myocardium malondialdehyde (MDA) level, and increased myocardium Na+-K+-ATPase, Ca2+-Mg2+-ATPase, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase (GR) activities. It can be concluded that ischemic postconditioning possesses strong protective effects against ischemia reperfusion-induced myocardium oxidative injury in IR rats.

摘要

短暂的心肌缺血-再灌注(IR)发作在长时间缺血后再灌注期间可能会减轻总缺血再灌注损伤。这种现象被称为缺血后处理。在本研究中,我们研究了缺血后处理对大鼠模型中缺血再灌注(IR)诱导的心肌氧化损伤的可能影响。结果表明,缺血后处理可以改善 IR 大鼠的心律失常,减少心肌梗死和血清肌酸激酶(CK)、乳酸脱氢酶(LDH)和天冬氨酸转氨酶(AST)的活性。此外,缺血后处理还可以降低心肌丙二醛(MDA)水平,增加心肌 Na+-K+-ATP 酶、Ca2+-Mg2+-ATP 酶、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)和谷胱甘肽还原酶(GR)的活性。可以得出结论,缺血后处理对 IR 大鼠的缺血再灌注诱导的心肌氧化损伤具有很强的保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a3c/6268873/02763e1d6f48/molecules-17-03805-g001.jpg

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