首页> 外文期刊>Molecules >Protective Effect of Ischemic Postconditioning against Ischemia Reperfusion-Induced Myocardium Oxidative Injury in IR Rats
【24h】

Protective Effect of Ischemic Postconditioning against Ischemia Reperfusion-Induced Myocardium Oxidative Injury in IR Rats

机译:缺血后处理对缺血再灌注所致IR大鼠心肌氧化损伤的保护作用

获取原文
           

摘要

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.
机译:长时间的缺血性损伤后再灌注期间发生的短暂性心肌缺血再灌注(IR)可能会减轻总的缺血再灌注损伤。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,缺血后处理可改善IR大鼠的心律失常,减轻心肌梗塞和血清肌酐激酶(CK),乳酸脱氢酶(LDH)和天冬氨酸转氨酶(AST)活性。此外,缺血后处理仍可降低心肌丙二醛(MDA)水平,并增加心肌Na + -K + -ATPase,Ca 2 + -Mg 2 + -ATPase,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)活性。可以得出结论,缺血后处理对IR大鼠缺血再灌注引起的心肌氧化损伤具有很强的保护作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号