Ischemic postconditioning improves the expression of cellular membrane connexin 43 and attenuates the reperfusion injury in rat acute myocardial infarction
机构:[1]Capital Med Univ, Beijing Anzhen Hosp, Dept Emergency Cardiol, 2 Anzhen Rd, Beijing 100029, Peoples R China;临床科室心脏内科中心首都医科大学附属安贞医院[2]China Japan Friendship Hosp, Dept Cardiol, Beijing 100029, Peoples R China;[3]Pudong New Area Dist Zhoupu Hosp, Dept Cardiol, Shanghai 201318, Peoples R China
To investigate the effects of cellular membrane connexin 43 (Cx43) and the potential details in ischemic postconditioning (IPOC) -induced cardioprotection, ischemia/reperfusion (IR) models were generated in 8-week-old male Sprague-Dawley rats by ligating the left coronary artery anterior descending branch. The serum levels of myocardial creatases, nitric oxide (NO) and malondialdehyde (MDA) levels, infarct size, arrhythmia events, expression and distribution of Cx43, ultrastructure and apoptosis in the myocardium in different treatments with IR, IR + IPOC, IR + diazoxide or IR + IPOC + 5-hydroxydecanoate acid (5-HD) were investigated. Consequently, IPOC decreased infarct size (10.9 vs. 43.3%, P< 0.01) and the levels of myocardial creatases, NO and MDA, and improved the expression (16.8 vs. 25.2% and 6.4 vs. 32.8%, after 1- and 3-h reperfusion, respectively; P< 0.01) and distribution of Cx43, ultrastructure and apoptosis (19.2 vs. 42.9%, P< 0.01) significantly. Diazoxide partly simulated the effects, and 5-HD attenuated but not completely abolished the effects of IPOC. In addition, the phosphorylated Cx43 (p-Cx43) level in the IR + IPOC group was lower than that in the IR + diazoxide group after 1-h reperfusion (26.1 vs. 29.4%, P> 0.05); however, it was reversed after 3-h reperfusion and the p-Cx43 level in the IR + IPOC group was significantly higher than that in the IR + diazoxide group (32.8 vs. 18.7%, P< 0.01). In conclusion, cell membrane Cx43 is also involved in the process of IPOC-induced cardioprotection and the improvement of membrane Cx43 is more dependent on mitochondrial K-ATP in the earlier phase of IPOC compared to the late phase of IPOC.
基金:
Development Funds of Capital Medicine [2009-3022]; Chinese Natural Science FoundationNational Natural Science Foundation of China [81100142]; Open Topic Funds Grants of Essential Laboratory in Cardiovasular Remodeling and Transforming Medicine, National Ministry of Education [2010XGCS02]; Cultivating Project Grants of Beijing for Highly Talented Men of Medicine [2014-3-042]; Superintendent Cultivating Funds Grants of Beijing Anzhen Hospital [2010F03]; Beijing Anzhen Hospital, Capital University of Medical Sciences; Beijing Institute of Heart Lung and Blood Vessel Diseases
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外文
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第一作者:
第一作者机构:[1]Capital Med Univ, Beijing Anzhen Hosp, Dept Emergency Cardiol, 2 Anzhen Rd, Beijing 100029, Peoples R China;
通讯作者:
通讯机构:[1]Capital Med Univ, Beijing Anzhen Hosp, Dept Emergency Cardiol, 2 Anzhen Rd, Beijing 100029, Peoples R China;
推荐引用方式(GB/T 7714):
He Hua,Li Nan,Zhao Zhihong,et al.Ischemic postconditioning improves the expression of cellular membrane connexin 43 and attenuates the reperfusion injury in rat acute myocardial infarction[J].BIOMEDICAL REPORTS.2015,3(5):668-674.doi:10.3892/br.2015.485.
APA:
He, Hua,Li, Nan,Zhao, Zhihong,Han, Fusheng,Wang, Xifu&Zeng, Yujie.(2015).Ischemic postconditioning improves the expression of cellular membrane connexin 43 and attenuates the reperfusion injury in rat acute myocardial infarction.BIOMEDICAL REPORTS,3,(5)
MLA:
He, Hua,et al."Ischemic postconditioning improves the expression of cellular membrane connexin 43 and attenuates the reperfusion injury in rat acute myocardial infarction".BIOMEDICAL REPORTS 3..5(2015):668-674