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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 invivo 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). Invitro, 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.
Highlights
Hypertension, arrhythmia, myocardial infarction (MI) and myocardial ischaemia/reperfusion (I/R) injury are all the most common cardiac diseases, which are the major causes of mortality in the world [1]
Our present study provides the first evidence that pulsed electromagnetic field (PEMF) has novel functions as follows: (1) We treated spontaneously hypertensive rats (SHR) rats with different PEMF intensity (8 min for 1 cycle, 30 +− 3 Hz, X-axis 0.22 +− 0.05 mT, Y-axis 0.20 +− 0.05 mT, Z-axis 0.06 +− 0.02 mT) 1–4 cycles per day for 7 days
(4) In vitro, PEMF treatment has a good effect on reducing reactive oxygen species (ROS) levels by protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS) pathway to release nitric oxide (NO) and improving cell apoptosis in neonatal rat cardiac ventricular myocytes (NRCMs) subjected to hypoxia
Summary
Hypertension, arrhythmia, myocardial infarction (MI) and myocardial ischaemia/reperfusion (I/R) injury are all the most common cardiac diseases, which are the major causes of mortality in the world [1]. Myocardial I/R injury is the most important cause of cardiac damage. After myocardium suffered severe ischaemia, restoration of the blood flow is a prerequisite for myocardial salvage [2]. Reperfusion may induce oxidative stress [4], inflammatory cell infiltration and calcium dysregulation [5]. All these players contribute to the heart damage such as contraction and arrhythmias [6], generally named
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