CAJ | 학술논문

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-KB(NF-KB)mRNA的表达水平(RT-PCR),同时观察心肌组织中自细胞介素-6(IL,6)、丙二醛(M13A)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,IP'IE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,AIX)P组的心肌梗死面积、NF一出mRNA的表达水平及Ⅱ,6、MI)A含量明显降低(K0.01),而SOD含量则显著升高(P<:0.01);而ADOP组与IPTC组相比,除NF桲B mRNA的表达及Ⅱ,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梤．B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.
목적 초보탐토선감후괄응대대서결혈재관주손상심기적보호작용급궤제.방법 48지건강웅성SD대서수궤분위4조:가수술조(Sham조)、결혈재관주조(IR조)、결혈후처리조(IPTC조)급선감후괄응조(ADOP조),매조12지,건립대서재체심기결혈재관주손상모형.실험종점측정심기경사면적(TTC염색),심기핵인자-KB(NF-KB)mRNA적표체수평(RT-PCR),동시관찰심기조직중자세포개소-6(IL,6)、병이철(M13A)급초양화물기화매(SOD)적함량변화,병행심기조직병이학검사.결과 Sham조심기조직형태개변불명현,IR조심기손상교중,IP'IE조급ADOP조중심기조직병이학손상교IR조명현감경.여IR조비교,AIX)P조적심기경사면적、NF일출mRNA적표체수평급Ⅱ,6、MI)A함량명현강저(K0.01),이SOD함량칙현저승고(P<:0.01);이ADOP조여IPTC조상비,제NF발B mRNA적표체급Ⅱ,6적분비초허강저(P<0.05)외,기타균무통계학차이(P>0.05).결론 선감후괄응가통과억제재관주후양자유기적과량생성급NF분．B활화소유도적조기염증반응,증강심기항양화능력,종이발휘보호효응.
Objective To investigate the protective effect and mechanism of adenosine postconditioning on myocardial ischemia-reperfusion injury inrats.Methods Forty-eight healthy male SD(Sprague-Dawley)rats were randomly divided into four groups(n=12 each):Sham group,IR(ischemiareperfusion)group,IPTC(ischemic postconditioning)group and ADOP(adenosine postconditioning)group to establish the rnodels of myccardial ischemia-measured at the end of ischemia-reperfusion,and light microscope was used to observe histopathological changes of myocardium.Results The injury to themyocardium was severe in the IR group,and the histopatbological changes of the myocardium were relieved obviously in both IPTC and ADOP groups.Thereconcentration of IL-6 in myocardial tissue decreased markedly(P＜0.01)in ADOP group,while the level of SOD increased significantly(P＜0.01).6 in ADOP group were a little lower than those in IPTC group(P＜0.05).Conclusion ADOP can increase antioxidant activity and inhibit the excretion of inflammatory factors induced by actived NF-кB after reperfusion to attenuate myocardi02 ischemia-reperfusion injury.Reduced the synthesis and release of oxygen free radicals and inhibited the inflammation induced by NF-кB at the early stage of myocardial ischemia reperfusion are involved in the mechanism.