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[1]覃琴,王琛,乔世刚,等.AMPK信号通路调控的自噬在七氟烷后处理保护大鼠心肌缺血再灌注损伤中的机制研究[J].生物医学工程研究,2016,01:36-40.
 QIN Qin,WANG Chen,QIAO Shigang,et al.Role of AMPK Signal Transduction Pathway in Protection Mechanism of Sevoflurane Postconditioning Protecting Rat Hearts against Myocardial Ischemia Reperfusion Injury in vivo[J].Journal of Biomedical Engineering Research,2016,01:36-40.
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AMPK信号通路调控的自噬在七氟烷后处理保护大鼠心肌缺血再灌注损伤中的机制研究(PDF)

《生物医学工程研究》[ISSN:1006-6977/CN:61-1281/TN]

期数:
2016年01期
页码:
36-40
栏目:
出版日期:
2016-03-25

文章信息/Info

Title:
Role of AMPK Signal Transduction Pathway in Protection Mechanism of Sevoflurane Postconditioning Protecting Rat Hearts against Myocardial Ischemia Reperfusion Injury in vivo
作者:
覃琴王琛乔世刚周迅△
苏州大学附属第二医院麻醉科,苏州215004
Author(s):
QIN Qin WANG Chen QIAO ShigangZHOU Xun
Department of Anesthesiology, Second Affiliated Hospital of SooChow University, Suzhou 215004, China
关键词:
腺苷酸活化蛋白激酶麻醉药吸入心肌缺血再灌注损伤自噬流
Keywords:
AMP-activated protein kinase Anesthetics inhalation Myocardial ischemia-reperfusion injury Autophagy
分类号:
R318
DOI:
-
文献标识码:
A
摘要:
研究七氟烷后处理对在体大鼠心肌缺血再灌注(I/R)损伤的保护作用,探讨腺苷酸活化蛋白激酶(AMPK)介导的自噬流在七氟烷后处理心肌保护中的作用。成年雄性SD大鼠50只,建立急性大鼠在体心肌I/R损伤模型。随机分为5组:假手术组(Sham组)、缺血再灌注组(I/R组)、七氟烷后处理组(SP组)、Compound c溶剂二甲基亚砜组(DMSO组)、AMPK抑制剂Compound c组(Com c组)。除Sham组,其余各组缺血30 min,再灌注4 h末。再灌注4 h末,提取心脏,采用氯化三苯基四氮唑染色法(TTC法)测定心肌梗死范围。采用免疫印迹法(Western blot技术)检测p-AMPK/t-AMPK、LC3 Ⅱ/Ⅰ及P62蛋白表达水平。与I/R组比较,SP组心肌梗死范围减小,p-AMPK/t-AMPK蛋白表达上调而LC3 Ⅱ/Ⅰ、P62蛋白表达下调(〖WTBX〗P〖WTBX〗<0.05);与〖WTBZ〗SP组比较,Com c组心肌梗死范围增加,p-AMPK/t-AMPK蛋白表达下调而LC3 Ⅱ/Ⅰ、P62蛋白表达上调(〖WTBX〗P〖WTBZ〗<0.05)。DMSO组相比于SP组差别无统计学意义(〖WTBX〗P〖WTBZ〗>0.05)。七氟烷后处理减轻了在体大鼠心肌I/R损伤,其机制可能是通过激活AMPK信号通路,减少再灌注期间自噬体的蓄积,保护自噬流进而发挥保护作用。
Abstract:
To investigate if sevoflurane postconditioning protecting rat hearts against ischemia-reperfusion injury in vivo by restoring impaired autophagosome clearance and the role of AMP-activated protein kinase (AMPK) signal transduction pathway in it. Fifty adult male Sprague-Dawley rats, weighing 270~320 g, were randomly divided into 5 groups(n=10 each): Sham operation group (Sham group), ischemia-reperfusion (I/R group), sevoflurane postonditioning group (SP group), sevoflurane postonditioning+selective AMPK inhibitor compound C group(Com c group) and compound C vehicle dimethyl sulfoxide(DMSO) group(DMSO group). Myocardial ischemia was induced by 30 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 4 h reperfusion, Myocardial infarct size was stained by triphenyltetrazolium chloride. Expression of p-AMPK/t-AMPK、LC3 Ⅱ/Ⅰand P62 were assessed by western blotting. Compared to I/R group, infarct size decreased and the expression of p-AMPK/t-AMPK was significantly up-regulated but LC3 Ⅱ/Ⅰand P62 protein were significantly down-regulated in SP group(〖WTBX〗P〖WTBZ〗<0.05); compared to SP group, infarct size increased and the expression of p-AMPK/t-AMPK was significantly down-regulated but LC3 Ⅱ/Ⅰand P62 protein were significantly up-regulated in Com c group(〖WTBX〗P〖WTBZ〗<0.05). Sevoflurane postcondition protects rat hearts against myocardial I/R injury in vivo, which may activatie AMPK signal transduction pathway and restoring impaired autophagosome clearance during myocardial reperfusion process.

参考文献/References

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备注/Memo

备注/Memo:
(收稿日期:2015-11-20)江苏省自然科学基金资助项目(BK20141187);苏州市科技计划项目(SYS201473);苏州大学附属第二医院博士、留学归国人员预研项目(SDFEYBS1401)通讯作者Email:double_qq@126.com
更新日期/Last Update: 2016-06-13