C反应蛋白对大鼠心肌细胞缺血再灌注损伤的影响及其机制  

The effects of C-reactive protein on myocardial ischemia reperfusion injury in rat cardiomyocytes and its mechanisms

作　　者：裴玮娜[1] 呼海娟[1] 刘凡[1] 鲁静朝[1] 杨秀春[1] 崔炜[1] PEI Weina;HU Haijuan;LIU Fan;LU Jingchao;YANG Xiuchun;CUI Wei(The Second Hospital of Hebei Medical University and Institute of Cardiocerebrovascular Disease of Hebei Province,Shijiazhuang050000,China)

机构地区：[1]河北医科大学第二医院.河北省心脑血管病研究所,石家庄050000

出　　处：《山东医药》2018年第33期39-42,共4页Shandong Medical Journal

基　　金：河北医学科学研究课题计划(20140073);河北医科大学第二医院科学研究基金项目(2h2201514)

摘　　要：目的探讨C反应蛋白(CRP)对大鼠心肌细胞缺血再灌注损伤的影响及其机制。方法应用SD乳鼠原代培养心肌细胞建立体外氧糖剥夺再灌注模型(OGD/R)。将心肌细胞采用CRP、环孢素A(CsA)、二氮嗪(DZ)进行不同处理后分为对照组、OGD/R组、CRP+OGD/R组、CRP+CsA+OGD/R组、CRP+DZ+OGD/R组。测定各组心肌细胞活力(设对照组细胞活力为100%)、细胞培养液乳酸脱氢酶(LDH)水平、线粒体膜通透性转换孔(m PTP)开放水平、线粒体膜电位水平。结果与OGD/R组相比,CRP+OGD/R组细胞活力下降、LDH水平升高、mPTP开放水平升高、线粒体膜电位水平降低,差异均有统计学意义(P均<0.05)。与CRP+OGD/R组相比,CRP+CsA+OGD/R组、CRP+DZ+OGD/R组细胞活力升高、LDH水平降低、mPTP开放水平降低、线粒体膜电位水平升高,差异均有统计学意义(P均<0.05)。结论 CRP的干预可以直接加重心肌缺血再灌注损伤,其机制可能与CRP能够降低线粒体膜电位水平,直接激活mPTP开放等有关。Objective To explore the effects of C-reactive protein(CRP)on myocardial ischemia reperfusion injury in rat cardiomyocytes and its mechanisms.Methods We simulated ischemia reperfusion using oxygen-glucose deprivation/reoxygenation(OGD/R)in neonatal Sprague-Dawley rat cardiomyocytes.Cardiomyocytes were treated with CRP,cyclosporine A(CsA),diazoxide(DZ)and divided into the control group,OGD/R group,CRP+OGD/R group,CRP+CsA+OGD/R group and CRP+DZ+OGD/R group.The myocardial cell viability,Lactic acid dehydrogenase(LDH)level in cell culture medium,mitochondrial membrane permeability transition pore(mPTP)opening level and mitochondrial membrane potential level were measured respectively.Cell viability was calculated as the percentage of the control group.Results Compared with the simple OGD/R group,the cell viability and mitochondrial membrane potential level decreased markedly,and the LDH leakage and mPTP opening level increased significantly in CRP+OGD/R group.All the differences were statistically significant(P<0.05).Compared with CRP+OGD/R group,in CRP+CsA+OGD/R group and CRP+DZ+OGD/R group,both cell viability and mitochondrial membrane potential level increased observably,and both LDH leakage and mPTP opening level reduced markedly.Conclusion Our results suggested that CRP directly aggravates myocardial ischemia reperfusion injury in myocardial cells and that this effect is primarily mediated by inhibiting mitoKATP channels and promoting mPTP opening.

关 键 词：缺血再灌注损伤 心肌细胞 C反应蛋白质 线粒体通透性转换孔 线粒体膜电位 大鼠 

分 类 号：R542.2[医药卫生—心血管疾病]