title: Novel protective effects of pulsed electromagnetic field ischemia/reperfusion injury rats.
abstract: Extracorporeal pulsed electromagnetic field (PEMF) has shown the ability to regenerate tissue by promoting cell proliferation. In the present study, we investigated for the first time whether PEMF treatment could improve the myocardial ischaemia/reperfusion (I/R) injury and uncovered its underlying mechanisms.In our study, we demonstrated for the first time that extracorporeal PEMF has a novel effect on myocardial I/R injury. The number and function of circulating endothelial progenitor cells (EPCs) were increased in PEMF treating rats. The in vivo results showed that per-treatment of PEMF could significantly improve the cardiac function in I/R injury group. In addition, PEMF treatment also reduced the apoptosis of myocardial cells by up-regulating the expression of anti-apoptosis protein B-cell lymphoma 2 (Bcl-2) and down-regulating the expression of pro-apoptosis protein (Bax). In vitro, the results showed that PEMF treatment could significantly reduce the apoptosis and reactive oxygen species (ROS) levels in primary neonatal rat cardiac ventricular myocytes (NRCMs) induced by hypoxia/reoxygenation (H/R). In particular, PEMF increased the phosphorylation of protein kinase B (Akt) and endothelial nitric oxide synthase (eNOS), which might be closely related to attenuated cell apoptosis by increasing the releasing of nitric oxide (NO). Therefore, our data indicated that PEMF could be a potential candidate for I/R injury.
authors: Department of Pharmacy, Shanghai Pudong Hospital, Fudan University, Shanghai 201399, China.
authors: Fenfen
authors: F
authors: Ma
authors: Shanghai Institute of Immunology & Department of Immunobiology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.|Shanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
authors: Wenwen
authors: W
authors: Li
authors: Shanghai Institute of Immunology & Department of Immunobiology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
authors: Xinghui
authors: X
authors: Li
authors: Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai 201203, China.
authors: Ba Hieu
authors: BH
authors: Tran
authors: Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai 201203, China.
authors: Rinkiko
authors: R
authors: Suguro
authors: Shanghai Institute of Immunology & Department of Immunobiology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
authors: Ruijuan
authors: R
authors: Guan
authors: Shanghai Institute of Immunology & Department of Immunobiology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
authors: Cuilan
authors: C
authors: Hou
authors: Longhua Hospital, Shanghai University of Tradition Chinese Medicine, Shanghai 201203,China.
authors: Huijuan
authors: H
authors: Wang
authors: Shanghai Institute of Immunology & Department of Immunobiology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
authors: Aijie
authors: A
authors: Zhang
authors: Shanghai Institute of Immunology & Department of Immunobiology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
authors: Yichun
authors: Y
authors: Zhu
authors: Longhua Hospital, Shanghai University of Tradition Chinese Medicine, Shanghai 201203,China zhuyz@fudan.edu.cn.|Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore 119228, Singapore.
authors: YiZhun
authors: Y
authors: Zhu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D004574:Electromagnetic Fields; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000628:therapy*; D032383:Myocytes, Cardiac / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D010766:Phosphorylation / Q000502:physiology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III; D051057:Proto-Oncogene Proteins c-akt
keywords: B-cell lymphoma 2 (Bcl-2); Bax; apoptosis; ischaemia/reperfusion (I/R) injury; pulsed electromagnetic field (PEMF)