文章摘要
赵 欣,沈 江,洪 涛,李 鑫,高 操,徐青荣.PARP⁃1在右美托咪定减轻大鼠心肌缺血再灌注损伤中的作用[J].南京医科大学学报,2019,(12):1723~1727
PARP⁃1在右美托咪定减轻大鼠心肌缺血再灌注损伤中的作用
Role of PARP⁃1 in attenuation of myocardial ischemia⁃reperfusion injury treated by dexmedetomidine in rats
投稿时间:2019-04-03  
DOI:10.7655/NYDXBNS20191204
中文关键词: 右美托咪定  心肌再灌注损伤  聚ADP核糖聚合酶类  凋亡  炎症介导素类
英文关键词: dexmedetomidine  myocardial reperfusion injury  poly(ADP⁃ribose)polymerases  apoptosis  inflammation mediators
基金项目:常州市卫生计生委指导性科技项目(WZ201810)
作者单位
赵 欣 苏州大学附属第三医院(常州市第一人民医院)麻醉科江苏 常州 213003 
沈 江 苏州大学附属第三医院(常州市第一人民医院)麻醉科江苏 常州 213003 
洪 涛 苏州大学附属第三医院(常州市第一人民医院)麻醉科江苏 常州 213003 
李 鑫 苏州大学附属第三医院(常州市第一人民医院)麻醉科江苏 常州 213003 
高 操 苏州大学附属第三医院(常州市第一人民医院)麻醉科江苏 常州 213003 
徐青荣 苏州大学附属第三医院(常州市第一人民医院)麻醉科江苏 常州 213003 
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中文摘要:
      目的:评价聚二磷酸腺苷核糖聚合酶?1(PARP?1)在右美托咪定减轻大鼠心肌缺血再灌注损伤中的作用。方法:健康清洁级雄性成年SD大鼠48只,体重200~240 g,8~12周龄,采用随机数字表法分为3组(n=16):假手术组(S组)、缺血再灌注组(I/R组)和缺血再灌注+右美托咪定组(I/R+Dex组)。S组仅开胸穿线不结扎;I/R组和I/R+Dex组采用结扎冠状动脉左前降支30 min恢复再灌注120 min的方法制备大鼠心肌缺血再灌注损伤模型;I/R+Dex组于再灌注前15 min腹腔注射右美托咪定5 μg/kg,S组和I/R组给予等容量生理盐水。分别于缺血前(T0)、缺血30 min(T1)、再灌注60 min(T2)和再灌注120 min(T3)时观察并记录平均动脉压(MAP)、心率(HR)和心率收缩压乘积(RPP);再灌注120 min时取左心室组织,称重并计算心肌梗死体积比率;采用Western blot法检测心肌组织PARP?1活化产物PAR和凋亡相关蛋白Caspase?3的表达;采用ELISA法测定心肌组织中TNF?α和IL?6的含量。结果:与T0时比较,I/R组和I/R+Dex组在T1~T3时MAP、HR和RPP水平降低(P<0.05);与S组比较,I/R组和I/R+Dex组在T1~T3时MAP、HR和RPP水平降低,梗死体积比率、TNF?α和IL?6含量升高,PAR和Caspase?3表达水平上调(P<0.05);与I/R组比较,I/R+Dex组在T1、T2时MAP、HR和RPP水平降低,T3时水平升高,梗死体积比率、TNF?α和IL?6含量降低,PAR和Caspase?3表达水平下调(P<0.05)。结论:右美托咪定可减轻大鼠心肌缺血再灌注损伤,机制与降低PARP?1活化抑制炎症和凋亡有关。
英文摘要:
      Objective:This study aims to evaluate the role of poly(ADP?ribose)polymerase?1(PARP?1)in attenuation of myocardial ischemia?reperfusion injury treated by dexmedetomidine in rats. Methods:Forty eight healthy male Sprague Dawley rats,8~12 weeks old,weighing 200~240 g were selected. The rats were then randomly divided into 3 groups(n=16):Sham operation group(S group),lung ischemia?reperfusion group(I/R group)and I/R+dexmedetomidine group(I/R+Dex group). In S group,the anterior descending branch was only exposed but not ligated;Myocardial I/R was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 120 min of reperfusion in I/R group and I/R+Dex group. Dexmedetomidine 5 μg/kg were injected intraperitoneally 15 min before reperfusion in I/R+Dex group while physiological saline was injected in S and I/R groups. The mean arterial pressure(MAP),heart rate(HR)and heart rate systolic blood pressure product(RPP)were observe and recorded before ischemia(T0),30 min of ischemia(T1) and reperfusion of 60 min(T2) and 120 min reperfusion(T3). At the end of 120 min reperfusion,hearts were removed for determination of the myocardial infarct size in the left ventricular myocardial tissues. The expression of PARP?1 activity markers(PAR)and apoptosis related protein Caspase?3 in myocardial tissue were investigated by Western blot. TNF?a and IL?6 levels were examined by ELISA. Results:Compared with the time point of T0,the MAP,HR and RPP were significantly decreased at time point of T1?T3 in I/R group and I/R+Dex group(P<0.05). Compared with S group,MAP,HR and RPP were significantly decreased at time point of T1?T3,myocardial infarct size,TNF?a and IL?6 levels,PAR and Caspase?3 expressions were increased in I/R group and I/R+Dex group(P<0.05). Compared with I/R group,MAP,HR and RPP were significantly decreased at time point of T1?T2 while increased at T3,myocardial infarct size,TNF?a and IL?6 levels,PAR and Caspase?3 expressions were decreased in I/R+Dex group(P<0.05). Conclusion:Dexmedetomidine can attenuate myocardial ischemia?reperfusion injury.The mechanism may be associated with reducing the activation of PARP?1,and then inhibit inflammation and apoptosis in myocardial tissue.
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