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(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(IcTnI)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);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。
Objective:To investigate the role of mitochondrial ATP-sensitive potassium channel(mito-KATP) in delayed sevoflurane preconditioning on 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 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 serum troponin I(cTnI) was detected at the end of reperfusion,and the myocardial infarct size(IS) was measured by triphenyltetrazolium chloride(TTC)staining.The levels of Ca2 +,malondialdehyde(MDA),superoxide dismutase(SOD),glutathione S-transferase(GST)and glutathione S-transferase Mu(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 myocardial ischemia-reperfusion,in which mito-KATP is an important regulator.
出处
《天津医药》
CAS
北大核心
2011年第8期739-742,共4页
Tianjin Medical Journal
基金
湖南省自然科学基金资助项目(项目编号:10JJ4021)
关键词
麻醉药
吸入
醚类
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
肌钙蛋白Ⅰ
丙二醛
超氧化物歧化酶
anesthetics
inhalation ethers myocardial reperfusion injury ischemic preconditioning
myocardial glutathione transferase mitochondrial proton-translocating atpases myocardial infarction troponinⅠ malondialdehyde superoxide dismutase