腺苷后适应对大鼠心肌缺血再灌注损伤的影响(英文)

Effects of adenosine postconditioning on the myocardial ischemia-reperfusion injury in rats

目的初步探讨腺苷后适应对大鼠缺血再灌注损伤心肌的保护作用及机制。方法48只健康雄性SD大鼠随机分为4组:假手术组(Sham组)、缺血再灌注组(IR组)、缺血后处理组(IPTC组)及腺苷后适应组(ADOP组),每组12只,建立大鼠在体心肌缺血再灌注损伤模型。实验终点测定心肌梗死面积(TTC染色),心肌核因子-κB(NF-κB)mRNA的表达水平(RT-PCR),同时观察心肌组织中白细胞介素-6(IL-6)、丙二醛(MDA)及超氧化物歧化酶(SOD)的含量变化,并行心肌组织病理学检查。结果Sham组心肌组织形态改变不明显,IR组心肌损伤较重,IPTC组及ADOP组中心肌组织病理学损伤较IR组明显减轻。与IR组比较,ADOP组的心肌梗死面积、NF-κBmRNA的表达水平及IL-6、MDA含量明显降低(P<0.01),而SOD含量则显著升高(P<0.01);而ADOP组与IPTC组相比,除NF-κBmRNA的表达及IL-6的分泌稍许降低(P<0.05)外,其他均无统计学差异(P>0.05)。结论腺苷后适应可通过抑制再灌注后氧自由基的过量生成及NF-κB活化所诱导的早期炎症反应,增强心肌抗氧化能力,从而发挥保护效应。

Objective To investigate the protective effect and mechanism of adenosine postconditioning on myocardial isehemia-reperfusion injury in rats. Methods Forty-eight healthy male SD （Sprague-Dawley） rats were randomly divided into four groups （n= 12 each）： Sham group, IR （ischemia reperfusion） group, IPTC （ischemic postconditioning） group and ADOP （adenosine postconditioning） group to establish the models of myocardial ischemiareperfusion injury. Myocardial infarct size （TTC staining）, NF-kB mRNA expression （RT PCR）, the concentration of IL-6 （ELISA）, MDA, SOD were all measured at the end of isehemia-reperfusion, and light microscope was used to observe histopathological changes of myocardiurn. Results The iniury to the myocardium was severe in the IR group, and the histopathological changes of the myoeardium were relieved obviously in both IPTC and ADOP groups. There were no changes observed in the sham group. Compared with IR group, myocardial Infarct tize, the expression of NF-kB rnRNA, the level of MDA, and the concentration of IL-6 in myocardial tissue decreased markedly （P〈0. 01 ） in ADOP group, while the level of SOD increased significantly （P〈0. 01 ）. However, the differences between ADOP group and IPTC group were not significant （ P〉0. 05）, except the expression of NF-kB mRNA and excretion of IL- 6 in ADOP group were a little lower than those in IPTC group （P〈20. 05）. Concusion ADOP can increase antioxidant activity and inhibit the excretion of inflammatory factors induced by actived NF-kB after reperfusion to attenuate myocardial ischemia-reperfusion injury. Reduced the synthesis and release of oxygen free radicals and inhibited the inflammation induced by NF-kB at the early stage of myocardial iscbernia reperfusion are involved in the mechanism.