摘要
目的探讨阿托伐他汀干预对缺血复合冷应激大鼠心肌的作用及可能机制。方法以永久性左冠状动脉前降支结扎术+4℃冷刺激(8 h/d,4 d)建立心肌缺血复合冷应激大鼠模型,复合应激前3天及后4天给以阿托伐他汀灌胃20 mg/(kg.d)。超声心动图评价心功能,TTC染色法测定心肌梗死面积,Western blot法检测心肌p-PI3K、p-GSK3β、Bim、Caspase3蛋白表达。结果心肌缺血复合冷应激使心功能恶化、梗死面积增大(P<0.01);阿托伐他汀干预后心功能改善、梗死面积缩小(P<0.01),p-PI3K、p-GSK3β表达上调(P<0.01),Bim、Caspase3表达下降(P<0.01)。结论阿托伐他汀可能经激活PI3K/Akt/GSK3β通路及下调Bim蛋白表达减轻缺血复合冷应激诱导的大鼠心肌损伤。
Objective To investigate the role of atorvastatin in myocardium of rats following co-stress of myocardial ischemia and cold stress,and the relative mechanism.Methods Co-stress model was developed by ligation of left coronary artery combined with cold stress of 4 ℃,8 h/d for 4 consecutive days.Rats were gavaged with atorvastatin 20 mg/（kg·d） for 3 days before MI was induced.Cardiac function was assessed by echocardiography;myocardial infarct size was determined by TTC staining;p-PI3K,p-GSK3β,Bim and Caspase-3 expression in myocardium was determined by western blotting.Results It was demonstrated that co-exposure to myocardial ischemia and cold stress could significantly deteriorate the cardiac function and increase the infarct size（P0.01）,and this was attenuated by atorvastatin with increased expression of p-PI3K,p-GSK3β,and Bim,Caspase3 downregulating（P0.01）.Conclusion Atorvastatin may attenuate cardiac injury induced by co-stress of myocardial ischemia and cold stress through activating PI3K/Akt/GSK3β pathway and decreasing expression of Bim.
出处
《基础医学与临床》
CSCD
北大核心
2011年第11期1200-1204,共5页
Basic and Clinical Medicine
基金
"十一五"国家科技支撑计划项目(2008BAI68B02)
