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p38MAPK信号通路在甘草酸二铵减轻兔心肌缺血再灌注损伤中的作用
引用本文:刘流,周海洋,冉珂,王建斌.p38MAPK信号通路在甘草酸二铵减轻兔心肌缺血再灌注损伤中的作用[J].南方医科大学学报,2010,30(2).
作者姓名:刘流  周海洋  冉珂  王建斌
作者单位:中南大学湘雅二医院麻醉科,湖南,长沙,410011
基金项目:湖南省科学技术厅基金资助项目(2009JT3018)
摘    要:目的观察p38MAPK信号通路在甘草酸二铵对兔心肌缺血再灌注损伤中的作用。方法30只新西兰大白兔随机分为3组,每组10只;假手术组(Ⅰ组)。缺血再灌注组(Ⅱ组)、甘草酸二铵处理组(Ⅲ组)。Ⅰ组行冠脉套线不阻断,Ⅱ、Ⅲ组均行后冠状动脉前降支阻断40min,再灌注120min。其中Ⅲ组在阻断前用甘草酸二铵2.5mg/kg静脉泵注。三组在阻断冠脉前20min(T0),阻断后20min(T1)、40min(T2)、再灌注后1h(T3)、2h(T4)取颈内动脉血测定血浆TNF-2、IL-6,IL-8细胞因子含量,再灌注结束后免疫印记法测心肌p38MAPK水平,再灌注结束后观察心肌细胞超微结构,同时用伊文思蓝和TIC染色法测心肌梗死面积。结果与Ⅱ组比较Ⅲ组p38MAPK表达降低(P<0.05),细胞炎性因子含量减少(P<0.05)。心肌细胞超微损伤减轻(P<0.05),心肌梗死面积减少(P<0.05)。结论甘草酸二铵通用下调心肌P38MAPK表达,减少炎性因子生成,抑制过度的炎性反应,改善心肌细胞超微结构,从而减轻心肌缺血再灌注损伤。

关 键 词:甘草酸二铵  缺血再灌注损伤  p38MAPK  心肌缺血  

Glylcyrrhiznatis ameliorates rabbit myocardial ischemia-reperfusion injury through P38MAPK pathway
LIU liu,ZHOU Hai-yang,RAN Ke,WANG Jiang-bin.Glylcyrrhiznatis ameliorates rabbit myocardial ischemia-reperfusion injury through P38MAPK pathway[J].Journal of Southern Medical University,2010,30(2).
Authors:LIU liu  ZHOU Hai-yang  RAN Ke  WANG Jiang-bin
Institution:LIU liu,ZHOU Hai-yang,RAN Ke,WANG Jiang-bin Department of Anesthesiology,Second Xiangya Hospital,Central South University,Changsha 410011,China
Abstract:Objective To investigate the role of p38MAPK pathway in the protective effect of glycyrrhiznatis against myocardial ischemia-reperfusion in rabbits.Methods Thirty rabbits were randomly divided into control group,I/R group,and glycyrrhiznatis group.In the latter two groups,the left anterior descending branch of the coronary artery was ligated for 40 min followed by 120 min of reperfusion,and in glycyrrhiznatis group,glycyrrhiznatis was given intravenously at 2.5 mg/kg before the occlusion.Blood samples were ...
Keywords:glycyrrhiznatis  ischemia-reperfusion injury  P38MAPK  myocardial ischemia  
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