UrocortinⅠ后处理对缺氧/复氧大鼠心肌线粒体膜电位的影响  

Effects of Urocortin I postconditioning on mitochondrial membrane potential during myocardial hypoxia / reoxygenation injury

作　　者：田伟[1] 顾燕[1] 邓胜利[1] 张琳[1] 

机构地区：[1]遵义医学院麻醉学系暨贵州麻醉与器官保护基础研究重点实验室,贵州遵义563099

出　　处：《遵义医学院学报》2015年第1期64-66,73,共4页Journal of Zunyi Medical University

基　　金：贵州省科学技术基金资助项目(NO:黔科合SY字[2013]3024)

摘　　要：目的探讨UrocortinⅠ后处理对缺氧/复氧后成年大鼠心肌细胞线粒体膜电位的影响。方法利用离体心脏灌注装置(MPA)分离成年大鼠心肌细胞,培养24 h后进行细胞计数并随机分为正常组(N组)、缺氧/复氧组(I/R组)、UrocortinⅠ后处理组(UcnⅠ组)、5-羟葵酸拮抗UrocortinⅠ组(5-HD+UcnⅠ组)。N组在预设37℃培养箱中持续培养135 min;余3组均予缺氧40 min,复氧60 min建立缺氧/复氧模型。其中UcnⅠ组在缺氧末复氧前给予UcnⅠ处理30 min;5-HD+UcnⅠ组在UcnⅠ处理前给予特异性线粒体ATP敏感性钾通道(mito-KATP)拮抗剂5-HD处理5 min,余处理同UcnⅠ组。各组于复氧末加入JC-1荧光探针并用激光共聚焦显微镜观察心肌细胞膜电位的变化。结果 N组心肌细胞高膜电位比例均高于其余各组(P<0.01),而UcnⅠ组高膜电位比例高于I/R组和5-HD+UcnⅠ组(P<0.05),I/R组与5-HD+Ucn I组比差异无统计学意义(P>0.05)。结论 UcnⅠ后处理可防止缺氧/复氧后心肌细胞线粒体膜电位的下降,保护复氧后心肌线粒体的膜电位。Objective To investigate the effects of mitochondrial membrane potential changes in Urocortin I - posteonditioning of myocardial hypoxia/reoxygenation injury. Methods Myocardial cells of adult rats were isolated using the MPA isolated heart - perfusion system. Myocardial cells were divided into four groups after 24 h cul- tures ： normal group （N） , hypoxia/reoxygenation group （I/R） , Urocortin I group （ Ucn I） , and 5 - hydroxyde- eanoate ＋ Uroeortin I group（5 - HD ＋ Ucn I）. The cells of group N was cultured continuously in the 37 ℃ in- cubator for 135 minutes while other groups experienced anoxia for 40 minutes and reoxygenation for 60 minutes to produce hypoxia/reoxygenation model. Ucn I group and group 5 - HD were given Ucn I - postconditioning for 30 minutes after hypoxia. 5 - HD was added to group 5 - HD ＋ Ucn I for 5 minutes before adding Ucn I. at the end of reoxygenation process. The cultured cardiomyoeytes were mixd with JC - 1 to detect the changes of mitochon- drial membrane potential by laser scanning confocal microscope. Results Normal group had the highest mitochon- drial membrane potential（ P 〈 0.05 ）while the potential of Uen I group is higher than that that in I/R group and 5 - HD ＋ Ucn I group （P 〈 0.05 ）. There was no significant difference between group I/R and group 5 - HD ＋ Uen I （P 〉 0.05 ）. Conclusion Ucn I - postconditioning could prevent the mitoehondrial membrane potential re-duction after myocardial cells suffer from hypoxia/reoxygenation and the mechanism may be mediated through the opening of mito - KATP channel.

关 键 词：UrocortinⅠ 后处理 缺氧/复氧 线粒体膜电位 心肌保护 

分 类 号：R614[医药卫生—麻醉学]