基础医学与临床 ›› 2011, Vol. 31 ›› Issue (11): 1200-1204.

• 研究论文 • 上一篇    下一篇

阿托伐他汀干预减轻缺血复合冷应激诱导的大鼠心肌损伤

黄茶花1,谢遥1,黄晓1,鲍晓明2,3,王耀晟4,程晓曙1   

  1. 1. 南昌大学第二附属医院心内科
    2.
    3. 南昌大学第二附属医院
    4. 南昌大学第二附属医院 南昌大学医学院心血管病研究所
  • 收稿日期:2011-03-07 修回日期:2011-03-31 出版日期:2011-11-05 发布日期:2011-11-02
  • 通讯作者: 程晓曙 E-mail:xiaoshumenfan@126.com
  • 基金资助:
    “十一五”国家科技支撑计划项目资助课题

Effect of atorvastatin on myocardial injury in rats following co-stress of myocardial ischemia and cold

  • Received:2011-03-07 Revised:2011-03-31 Online:2011-11-05 Published:2011-11-02

摘要: 摘要:目的 分析缺血复合冷应激对大鼠心肌的影响,探讨阿托伐他汀干预对这种复合应激下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小时/天,4天)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(20mg.kg-1.d-1)。超声心动图评价心功能,TTC染色法测定心肌梗死面积,western blotting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 心肌缺血复合冷应激加重心肌损伤,阿托伐他汀干预能部分减弱此作用,其机制可能与激活PI3K/Akt/GSK3β通路及下调Bim表达有关。

关键词: 心肌梗死, 冷刺激, 阿托伐他汀, Bim

Abstract: Abstract: Objective To analyze the effect of co-stress of myocardial ischemia(MI) and cold on myocardium in rats,and investigate the role and relative mechanism of atorvastatin intervention in such co-stress.Methods Co-stress model was induced by ligation of left coronary artery combined with cold stress of 4℃,8h/d for 4 consecutive days.Rats were gavaged with atorvastatin 20mg.kg-1.d-1 for 3 days before MI was induced and thereafter for 4 days.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 of myocardial ischemia and cold stress could significantly deteriorate the cardiac function and increase the infarct size (P<0.01),and this was attenuated by atorvastatin use with increased expression of p-PI3K,p-GSK3β and Bim, Caspase3 downregulating(P<0.01).Conclusion Co-exposure to myocardial ischemia and cold stress aggravate the cardiac injury, this influence can partially attenuated by atrovastatin use and the mechanism may be attributed to activation of PI3K/Akt/GSK3β and decreasing expression of Bim.

Key words: myocardial infarction, cold stress, atorvastatin, Bim