CAJ | 학술논문

目的探讨缺血后处理对在体兔心肌缺血再灌注心肌细胞凋亡和线粒体结构与功能的影响以及可能机制.方法 80只兔随机分为假手术组(sham组)、心肌缺血再灌注组(IR组)、缺血预处理组(IP组)、缺血后处理组(PC组)以及缺血后处理加5-羟葵酸(5-HD)干预组(PC+5-HD组).用TUNEL法检测心肌细胞凋亡,用透射电镜观察心肌细胞的超微结构,用荧光法检测线粒体膜电位,比色法测线粒体Ca~(2+)浓度、丙二醛(MDA)浓度、超氧化物岐化酶(SOD)活性.结果与IR组比较,PC组和IP组兔心肌细胞凋亡减少,心肌及线粒体形态结构改变明显减轻,线粒体跨膜电位、SOD活性明显升高、线粒体Ca~(2+)浓度、MDA浓度均下降(P<0.05),5-HD部分降低上述作用.结论 PC可能通过提高线粒体跨膜电位、降低线粒体氧自由基水平、减轻线粒体钙超载而减轻心肌细胞损伤,其机制可能与线粒体功能损伤有关.
목적 탐토결혈후처리대재체토심기결혈재관주심기세포조망화선립체결구여공능적영향이급가능궤제.방법 80지토수궤분위가수술조(sham조)、심기결혈재관주조(IR조)、결혈예처리조(IP조)、결혈후처리조(PC조)이급결혈후처리가5-간규산(5-HD)간예조(PC+5-HD조).용TUNEL법검측심기세포조망,용투사전경관찰심기세포적초미결구,용형광법검측선립체막전위,비색법측선립체Ca~(2+)농도、병이철(MDA)농도、초양화물기화매(SOD)활성.결과 여IR조비교,PC조화IP조토심기세포조망감소,심기급선립체형태결구개변명현감경,선립체과막전위、SOD활성명현승고、선립체Ca~(2+)농도、MDA농도균하강(P<0.05),5-HD부분강저상술작용.결론 PC가능통과제고선립체과막전위、강저선립체양자유기수평、감경선립체개초재이감경심기세포손상,기궤제가능여선립체공능손상유관.
Objective To investigate the effects of ischemic postconditioning on apoptosis, structural and functional changes of mitochondria induced by myocardial isehemia/reperfusion (I/R) injury of rabbits and potential mechanism. Methods Eighty healthy rabbits were divided randomly into five groups: sham operation group ( Group Sham) , ischemic reperfusion group (Group IR) , ischemic preconditioning group (Group IP) , ischemic postconditioning group (Group PC) and 5-HD plus ischemic postconditioning group (Group PC +5-HD). All rabbits in the five groups were killed 4 h after reperfusion. The hearts were quickly collected for microscopy by TUNEL. We observed ultrastructural changes of myocardium under electron microscope and examined mitochondrial membrane potential and Ca~(2+) concentration, MDA content and SOD activity of myocardial mitochondria. Results Compared with group IR, the damage of mitoehondrial ultrastrueture was milder, the apoptosis rate decreased and Ca concentration and MDA content were much lower in group IP and group PC ( P < 0. 05 ). Mitochondrial membrane potential and SOD activity of myocardial mitochondria in group IP and group PC was significantly higher than that in group IR(P<0.05). The protective effect of PC against I/R injury was partially counteracted by 5-HD .Conclusion Ischemic posteonditioning can protect the heart from I/R injury, this is supported by improvement mitochondrial ultrastructure and by decreasing apoptosis, increasing mitochondrial membrane potential and SOD activity, alleviating Ca~(2+) overload and decreasing MDA content in myocardial mitochondria. The cardio protective effects may be explained by mitochondrial ATP sensitive potassium channel.