摘要
目的:给予罗格列酮(ROS)预处理并且诱导大鼠心肌缺血预适应后,观察心肌梗死面积以及脂联素的分泌,探讨缺血预适应中脂联素的保护机制。方法:用随机数字发生器将SD雄性大鼠随机分为4组:①缺血再灌注组(I/R组);②缺血预适应组(IPC组);③罗格列酮+缺血再灌注组(ROS+I/R组);④罗格列酮+缺血预适应组(ROS+IPC组),各8只。通过RT-PCR测定大鼠心脏脂联素含量。测定大鼠心脏心肌梗死面积,观察脂联素含量。结果:ROS+IPC组脂联素的表达水平分别与ROS+I/R组、IPC组及I/R组相比,差别有显著统计学意义(P<0.01)。结论:罗格列酮增加了脂联素的分泌,使其mRNA表达水平增高,减少了心肌梗死面积。这可能是罗格列酮在IPC中产生对心肌保护的主要机制之一。
Objective：To explore the effect of rosiglitazone（rosiglitazone,ROS）in ischemic preconditioning of myocardium.induced myocardial preconditioning and ischemic preconditioning,we observed the myocardial infarct size and adiponectin secretion of ischemic preconditioning in the protection mechanisms of adiponectin.Method：The 32SD male rats were randomly divided into 4groups by random number generator：①ischemia reperfusion group（I/R group）;②ischemic preconditioning group（IPC group）;③rosiglitazone＋ischemia-reperfusion Group（ROS ＋I/R group）;④rosiglitazone＋ischemic preconditioning group（ROS＋IPC group）.Myocardial preconditioning and ischemic preconditioning animal model was induced in rat.We measured the levels of adiponectin by RT-PCR in rat heart,and observed the myocardial infarct size in rat heart on myocardial ischemia.Result：In the ROS＋IPC group,the adiponectin mRNA expression was significantly increased in the ROS＋I/R group,IPC group and I/R group.Conclusion：Rosiglitazone could increase adiponectin secretion,and reduce myocardial infarct size.
出处
《临床心血管病杂志》
CSCD
北大核心
2014年第1期34-36,共3页
Journal of Clinical Cardiology
关键词
罗格列酮
脂联素
缺血再灌注
缺血预适应
rosiglitazone
adiponectin
ischemia-reperfusion
ischemic preconditioning
