天津医药

• 实验研究 • 上一篇    下一篇

Mito-KATP在七氟醚延迟预处理减轻大鼠心肌缺血再灌注氧化损伤中的作用

肖艳英1,常业恬1,冉珂2,李双凤1   

  1. 1. 中南大学湘雅二医院
    2. 中南大学湘雅二医院麻醉科
  • 收稿日期:2010-12-06 修回日期:2011-03-12 出版日期:2011-08-15 发布日期:2011-08-15
  • 通讯作者: 肖艳英

Role of Mito-KATP in Delayed Preconditioning with Sevoflurane Reducing Oxidative Injury Induced by Myocardial Ischemia-Reperfusion in Rats

  • Received:2010-12-06 Revised:2011-03-12 Published:2011-08-15 Online:2011-08-15
  • Contact: Yan-Ying XIAO

PDF (PC)

2018

摘要： 目的：探讨线粒体ATP敏感性钾通道（mito-KATP）在七氟醚延迟预处理减轻大鼠心肌缺血再灌注氧化损伤中的作用。方法：健康雄性SD大鼠60只随机分为5组（n =12）：假手术组（Sham组）、缺血再灌注组（IR组）、七氟醚预处理组（SPC组）、七氟醚预处理+ 5-羟基癸酸组（SPC+5-HD组）和5-羟基癸酸组（5-HD组）。灌注结束时检测血清肌钙蛋白I（cTnI）浓度，氯化三苯四氮唑（TTC）染色确定心肌梗死面积。检测心肌丙二醛（MDA）、Ca2+含量、超氧化物歧化酶（SOD）、谷胱甘肽硫转移酶（GST）活性以及谷胱甘肽硫转移酶Mu（GSTM）表达。 结果： IR组较Sham组心肌梗死面积和cTnI释放增加，心肌MDA含量和Ca2+浓度增加，SOD、GST活性和心肌GSTM表达增加（P < 0.01）； SPC组较IR组心肌梗死面积和cTnI释放减少，心肌MDA含量和Ca2+水平也减少，SOD和GST活性以及心肌GSTM增加（P < 0.01）；SPC+5-HD组较SPC组心肌梗死面积和cTnI释放增加，心肌MDA含量和Ca2+浓度增加，SOD、GST活性和心肌GSTM表达降低（P <0.01）。结论：七氟醚延迟预处理能减轻大鼠心肌缺血再灌注所致氧化损伤， mito-KATP在其中起调节作用。

关键词: 麻醉药, 吸入, 心肌再灌注损伤, 缺血预处理, 心肌, 谷胱甘肽转移酶, 线粒体质子转运ATP酶, 心肌梗死

Abstract: Objective：To investigate the role of mitochondrial ATP-sensitive potassium channel (mito-KATP) in delayed preconditioning with sevoflurane reducing oxidative injury induced by myocardial ischemia-reperfusion in rats. Methods：Sixty healthy male SD rats were randomly divided into 5 groups (n = 12): the sham operating group (Sham), the ischemia-reperfusion group (IR), the sevoflurane preconditioning group ( SPC), the sevoflurane preconditioning + 5-hydroxydecanoate group (SPC +5-HD)and the 5-hydroxydecanoate group (5-HD). Serum cTnI were detected at the end of reperfusion and myocardial infarct size(IS) were measured by triphenyltetrazolium chloride（TTC）staining. The Ca2 + levels and malondialdehyde (MDA) content in the myocardium were determined. The activity of superoxide dismutase (SOD) and glutathione S-transferase (GST) was measured. Western blot assay was used to assess the expression of glutathione S-transferase Mu (GSTM) expression in the left ventricle. Results： After ischemia-reperfusion,IR group indicated a significant increase of infarct size ,serum cTnI release, myocardial MDA and Ca2+ content, but a decreased activity of SOD, GST and myocardial GSTM expression (P＜0.01).SPC attenuated the infarct ratio and cTnI release, down-regulated myocardial MDA and Ca2+levels， but up-regulated SOD and GST activity and myocardial GSTM abundance(P＜0.01). As compared with SPC group, SPC+5-HD group increased infarct size, serum cTnI levels, myocardial MDA and Ca2+ content, but decreased SOD , GST activity and myocardial GSTM (P<0.01). Conclusion：Delayed preconditioning with sevoflurane can reduce oxidative injury induced by myocardial ischemia-reperfusion, in which mito-KATP is an important regulator.

Key words: anesthetics, inhalation, myocardial reperfusion injury, ischemic preconditioning, myocardial, glutathione transferase, mitochondrial proton-translocating atpases, 心肌梗死