缺血后处理对大鼠心肌缺血/再灌注不同时相损伤营救激酶及线粒体通透性转换孔的影响  

Effect of Ischemic Postconditioning on the Reperfusion Injury Salvage Kinase and Mitochondrial Permeability Transition Pore at Different Time Phases of Myocardial Ischemia-reperfusionon in Rats

作　　者：肖军 黎立 姜振宇 史迎昌 孙佳增 刘维全[4] 孙慧娜 陶耀兵 

机构地区：[1]解放军第三○九医院心内科 [2]北京新技术公司,100091 [3]解放军第三○九医院动物实验中心 [4]中国农业大学生物学院,北京100091

出　　处：《医学综述》2015年第5期890-892,共3页Medical Recapitulate

基　　金：北京市自然科学基金(7122178)

摘　　要：目的探讨缺血后处理对大鼠心肌缺血/再灌注不同时相损伤营救激酶及线粒体通透性转换孔(m PTP)的影响。方法建立近交系Lewis大鼠颈部异位心脏移植左心作功模型,120只受体大鼠存活2 d后,采用随机数字表法分为移植心脏缺血/再灌注组、缺血后处理组和假手术组,其中假手术组8只,其余两组分别为56只,每个时相点8只,在再灌注3、6、12、24 h及2、4、7 d分别检测移植心脏心肌细胞磷酸化蛋白激酶(p-AKT)、细胞外信号调节激酶1/2(p-ERK1/2)蛋白表达、m PTP开放程度和心肌梗死范围。结果在再灌注的7个时相点,缺血后处理组与再灌注组心肌细胞p-AKT与p-ERK1/2蛋白表达及m PTP开放程度对应比较,差异均有统计学意义(均P<0.05),两组蛋白表达及m PTP开放程度均明显高于假手术组(均P<0.05);缺血后处理组心肌梗死范围显著小于再灌注组(P<0.05或P<0.01)。结论缺血后处理在大鼠移植心脏心肌缺血/再灌注3 h至7 d内能有效升高心肌细胞p-AKT、p-ERK1/2蛋白的表达,抑制心肌细胞m PTP开放,缩小心肌梗死范围。Objective To explore the effects of ischemic postconditioning on the reperfusion injury sal-vage kinase and the opening of mitochondrial permeability transition pore（mPTP） at different time phases of myocardial ischemia-reperfusion injury in rats.Methods Isogenic adult Lewis rat models of cervical hetero-topic and working-heart transplantation were established.The 120 recipients were divided into ischemia-reperfusion group,ischemic postconditioning group and sham operation group ,8 rats in the sham operation group, 56 in the other two groups respectively,8 for each time phase point.Myocardial infarction size,expres-sion of p-AKT and p-ERK1/2 protein and the opening of mPTP were measured respectively at 3, 6, 12,24-hour and 2,4, 7-day after reperfusion.Results The expression of p-AKT and p-ERK1/2 protein and the opening of mPTP were statistically significant different between the ischemia-reperfusion group and ischemic postconditioning group at 7 time points after reperfusion（P〈0.05）,while both of which were higher than the sham operation group.The myocardial infarction range of the postconditioning group was less than the ische-mia-reperfusion group（P 〈0.05）.Conclusion Ischemic postconditioning can increase the expression of p-AKT and p-ERK1/2 protein,decrease the opening of mPTP and myocardial infarction range between 3 hours and 7 days after the reperfusion after myocardial ischemia in rats .

关 键 词：缺血后处理 缺血/再灌注损伤 心肌/再灌注损伤营救激酶 线粒体通透性转换孔 

分 类 号：R541.4[医药卫生—心血管疾病]