Novel protective effects of pulsed electromagnetic field ischemia/reperfusion injury rats. Issue 6 (5th December 2016)

• Record Type: Journal Article
• Authors: Ma, Fenfen; Li, Wenwen; Li, Xinghui; Tran, Ba Hieu; Suguro, Rinkiko; Guan, Ruijuan; Hou, Cuilan; Wang, Huijuan; Zhang, Aijie; Zhu, Yichun; Zhu, YiZhun
• Is Part Of: Bioscience reports. Volume 36:Issue 6(2016)
• Publication Date: 2016-12-05
• Subjects: apoptosis -- Bax -- B-cell lymphoma 2 (Bcl-2) -- ischaemia/reperfusion (I/R) injury -- pulsed electromagnetic field (PEMF); Molecular biology -- Periodicals; Cytology -- Periodicals; 572.8
• DOI: 10.1042/BSR20160082
• Languages: English
• ISSNs: 0144-8463

Abstract

Abstract : Pulsed electromagnetic field (PEMF) treatment protected ischaemia/reperfusion (I/R) injury from apoptosis via B-cell lymphoma 2 (Bcl-2), Bax and nitric oxide (NO) releasing. 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.