Acupuncture pretreatment protects heart from injury in rats with myocardial ischemia and reperfusion via inhibition of the β1-adrenoceptor signaling pathway

被引:80
作者
Gao, Junhong
Fu, Weixing
Jin, Zhigao
Yu, Xiaochun
机构
[1] Chinese Acad Med Sci, Dept Physiol, Expt Res Ctr, Beijing 100700, Peoples R China
[2] Chinese Acad Med Sci, Dept Physiol, Inst Acupuncture, Beijing 100700, Peoples R China
基金
中国国家自然科学基金;
关键词
electro-acupuncture; pretreatment; ischemic injury; beta(1)-adrenoceptor; signal transduction;
D O I
10.1016/j.lfs.2007.01.019
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Our previous study showed that a cardioprotective effect was produced by pretreatment with acupuncture at bilateral Neiguan acupoints (PC6) and the effect of EA was diminished by propranolol, a nonspecific antagonist of beta-adrenoceptors (beta-ARs) which are the most powerful cardiac receptors, indicating an involvement of beta-ARs. The present study explored further the signaling mechanism underlying the cardioprotective effect of acupuncture pretreatment in rats subjected to myocardial ischemia and reperfusion (MIR). Myocardial ischemia was achieved by ligating the left anterior descending coronary artery and reperfusion by releasing the ligation. Adult rats were divided into three groups, namely, a normal control (NC) group, a group subjected to ischemia and reperfusion (IR) only, and a group given electro-acupuncture (EA) before IR. For EA, bilateral Neiguan points (PC6) of the rats were stimulated for 30 min once a day for 3 consecutive days. The ST segment of ECG, the ratio of infarct size over risk zone, and the contents of beta(1)-adrenoceptor (beta(1)-AR), Gsa protein and cAMP in ischemic myocardium were compared among the three groups. IR increased the elevation of ECG ST segment, myocardial infarct size, contents of beta(1)-AR, Gs alpha protein and cAMP. These effects were attenuated by EA pretreatment at bilateral Neiguan acupoints. In conclusion, the present results indicate that EA produces cardioprotective effect against IR which may be mediated via the beta(1)-AR-Gs-protein-cAmp pathway. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:1484 / 1489
页数:6
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