依达拉奉对缺氧/复氧损伤诱导心肌细胞凋亡的影响  

Effects of edaravone on apoptosis induced by hypoxia/reoxygenation in cardiocytes

作　　者：何勇[1,2] 李战宁[2] 耿希刚[1] 

机构地区：[1]西安交通大学医学院第一附属医院心脏外科,陕西西安710061 [2]武警陕西总队医院心脏外科,陕西西安710054

出　　处：《西安交通大学学报（医学版）》2013年第4期490-494,共5页Journal of Xi’an Jiaotong University（Medical Sciences）

摘　　要：目的观察依达拉奉(EDA)对缺氧/复氧(H/R)损伤诱导的原代培养的新生大鼠心肌细胞凋亡的影响。方法用原代培养的新生大鼠心肌细胞在体外建立心肌缺血再灌注损伤模型,分为正常组、H/R组和EDA预处理+H/R组,应用CCK-8比色法检测细胞存活率;DAPI染色法和流式细胞仪PI标记法检测细胞凋亡率;同时检测乳酸脱氢酶(LDH)、肌酸激酶(CK)和超氧化物歧化酶(SOD)的活性以及丙二醛(MDA)、活性氧(ROS)和还原型谷胱甘肽/氧化型谷胱甘肽(GSH/GSSG)含量。结果 H/R组心肌细胞存活率明显下降,凋亡率明显升高(P<0.05),40μmol/L的EDA预处理1h明显抑制H/R处理诱导的细胞存活率下降和凋亡率升高(P<0.05)。同时,H/R组LDH和CK的活性以及MDA、ROS、GSH含量和GSH/GSSG比值显著升高(P<0.05),而SOD的活性明显下降(P<0.05);与H/R组相比,EDA预处理后LDH与CK的活性、MDA、ROS、GSH含量和GSH/GSSG比值明显降低(P<0.05),SOD的活性明显升高(P<0.05)。结论 EDA预处理可以减少H/R诱导的心肌细胞凋亡,可能与其抗氧化作用有关。Objective To investigate the effects of edaravone on apoptosis induced by hypoxia/reoxygenation（H/R） in primary cultured rat cardiocytes.Methods Myocardial ischemia-reperfusion injury was mimicked in primary cultured rat cardiocytes by H/R injury.The cells were divided into normal group,H/R group and EDA＋H/R group.Cell survival rate was detected by chromatometry with Cell Counting Kit-8.Cell apoptosis rate was detected using DAPI staining and flow cytometry.Meanwhile,the levels of lactate dehydrogenase（LDH）,creatine kinase（CK） and superoxide dismutase（SOD） activities,as well as the contents of malondialdehyde（MDA）,radical oxygen species（ROS） and reduced/oxidized glutathione（GSH/GSSG） were assayed.Results Cell survival rate was significantly decreased in H/R group with an increased apoptosis rate（P0.05）.Pre-treatment with edaravone with a concentration of 40 μmol/L could significantly attenuate the decrease in cell survival rate and increase in apoptosis rate（P0.05）.Compared to those in normal group,the levels of LDH and CK activities,the contents of MDA,ROS and GSH,as well as the rate of GSH/GSSG were significantly increased in H/R group（P0.05）.However,the level of SOD activities was decreased in H/R group compared with that in the normal group（P0.05）.In EDA＋H/R group,the levels of LDH and CK activities,the contents of MDA,ROS and GSH,as well as the rate of GSH/GSSG were significantly decreased compared to those in H/R group（P0.05）,with a significant increase in the level of SOD activities（P0.05）.Conclusion Edaravone pre-treatment can decrease hypoxia/reoxygenation-induced apoptosis of primary cultured neonate rat cardiocytes,in which anti-oxidation system may be involved.

关 键 词：依达拉奉 心肌细胞 缺血再灌注损伤 凋亡 氧化应激 超氧化物歧化酶(SOD) 丙二醛(MDA) 活性氧(ROS) 

分 类 号：R363[医药卫生—病理学]