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

摘要

目的:探讨线粒体ATP敏感性钾通道(mito-K_ATP)在七氟醚延迟预处理减轻大鼠心肌缺血再灌注(IR)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(Sham)组、IR组、七氟醚预处理(SPC)组、七氟醚预处理+5-羟基癸酸(SPC+5-HD)组和5-羟基癸酸(5-HD)组.灌注结束时检测血清肌钙蛋白I (cTnl)水平,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cTnl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); 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cTnl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-K--ATP在其中起调节作用.%Objective :To investigate the role of mitochondrial ATP-sensitive potassium channel (mito-KATP) in delayed sevoflurane preconditioning on reducing oxidative injury induced by nyocardial ischemia-reperfusion in rats. Methods: Sixty healthy male SD rats were randomly divided into 5 groups (n=12), the sham 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). The level of serun troponin I(cTnI) was detected at the end of reperfusion,and the myocardial infarct size(IS) was measured by triphenyItetrazolium chloride (TTC)staining. The levels of Ca2+, malondialdehyde (MDA), superoxide dismutase (SOD),glutathione S-transferase (GST)and glutathione S-transferase Mn (GSTM) in the myocardium were determined. Results: After ischemia-reperfusion, there were significant increases in infarct size ,serum cTnI release, myocardial MDA and Ca2+ content in IR group compared with those of Sham group(P ＜ 0.01). But there were decreased infarct size, serum cTnI release, myocardial MDA and Ca2+ content, and up-regulated activity of SOD, GST and myocardial GSTM expression in SPC group than those of IR group(P ＜ 0.01). Also there were increased infarct size, serum cTnI release, myocardial MDA and Ca2+ content, and down-regulated activity of SOD, GST and myocardial GSTM expression in SPC+5-HD group than those of SPC group (P ＜ 0.01 ). Conclusion :The delayed preconditioning with sevoflurane can reduce oxidative injury induced by myoeardial isehemia-reperfusion, in which mito-KATP is an important regulator.