法舒地尔通过调节线粒体膜通透性转换孔的开放减少大鼠缺血再灌注心肌损伤  

Fasudil maybe perform its protection effect on rat heart suffering from ischemia-reperfusion injury by regulating the opening of mitochondrial permeablity transition pore

作　　者：邓宇珺[1] 谭宁[2] 马建超[3] 符永恒[4] 曾红科[1] 

机构地区：[1]广东省人民医院(广东省医学科学院)急危重症医学部,广州510080 [2]广东省心血管病研究所心内科广东省人民医院(广东省医学科学院),广州510080 [3]广东省人民医院(广东省医学科学院)肾内科,广州510080 [4]广东省人民医院(广东省医学科学院)医学研究中心,广州510080

出　　处：《岭南心血管病杂志》2016年第3期332-336,共5页South China Journal of Cardiovascular Diseases

基　　金：广东省医学科研基金(项目编号:A2013006);广东省医学科研基金(项目编号:A2013021)

摘　　要：目的通过观察法舒地尔及线粒体膜通透性转换孔(mitochondrial permeablity transition pore,MPTP)开放剂苍术苷干预下大鼠缺血再灌注心肌的坏死和凋亡情况,探讨法舒地尔是否通过调节MPTP的开放减轻大鼠缺血再灌注心肌损伤。方法 25只Sprague-Dawley(SD)雄性大鼠按随机数字表法随机分为5组(每组5只),除了空白对照组外,建立在体大鼠心肌缺血再灌注模型(缺血35 min,再灌注120 min)。分别予以法舒地尔(0.5 mg/kg)、苍术苷(5 mg/kg)、法舒地尔+苍术苷干预。用3,5一氧化三苯基四氮唑(TTC)检测大鼠心肌梗死面积,末端脱氧核糖核苷酸转移酶介导的dUTP缺口末端标记法(TdT-mediated dUTP nick end labeling,TUNEL)法检测大鼠心肌凋亡。结果法舒地尔组的心肌梗死面积明显比缺血再灌注组的减少,差异有统计学意义(22%±8.2% vs.41%±6.4%,P<0.05);苍术苷组的心肌梗死面积与缺血再灌注组的比较,差异无统计学意义(P>0.05);法舒地尔+苍术苷心肌梗死面积比法舒地尔组的增大,两者比较差异有统计学意义(32%±8.5% vs.22%±8.2%,P<0.05)。与缺血再灌注组比较,法舒地尔组心肌细胞凋亡细胞数下降,差异有统计学意义(10.3±4.5 vs.18.7±5.4,P<0.05);法舒地尔+苍术苷组心肌细胞凋亡指数比法舒地尔组大,差异有统计学意义(13.5±5.2 vs.10.3±4.5,P<0.05)。结论法舒地尔可能通过调节MPTP的开放减少大鼠缺血再灌注心肌损伤。Objectives To study whether fasudil perform its protection effect on rat heart suffering from isehemia- reperfusion injury by regulating the opening of mitochondrial permeablity transition pore （MPTP） in vivo. Methods Twenty-five male Sprague-Dawley rats were randomly divided into 5 groups： sham operation （SHAM） group, ischemia- reperfusion （I/R） group, fasudil group, atraetyloside group and fasudil＋atraetyloside group. Rat model of myocardial isehemia-repeffusion injury was established by ligation of the left anterior descending coronary artery for 35 minutes and subsequent reperfusion 120 minutes. The heart infarct size was determined with three phenyl tetrazole chloride （TrC） staining. The myocardial cell apoptotie index （AI） was determined with terminal deoxynueleotidyl transferase mediated dUTP-biotin nick end-labeling （TUNEL） method. Results There was no myocardial infarction in SHAM group, while the cardiac infarct size was 41%±6.4%, 22%±8.2%, 42%±7.4% and 32%±8.5% in I/R, fasudil, atractyloside, and fasudil＋atractyloside group, respectively, with significant differences revealed among the five groups （P〈0.05）. Meanwhile, AI was 2.5%±1.2%, 18.7%±5.4%, 10.3%±4.5%, 19.2%±6.2% and 13.5%±5.2% in SHAM , I/R, fasudil, atractyloside, and fasudit＋atractyloside group, respectively, with significant differences revealed among the five groups （P〈0.05）. Conclusions Fasudil maybe perform its protection effect on rat heart suffering from ischemia- reperfusion injury by regulating the opening of MPTP.

关 键 词：心肌缺血再灌注损伤 法舒地尔 线粒体膜通透性转换孔 

分 类 号：R542[医药卫生—心血管疾病]