title: Protective effects of low-frequency magnetic fields on cardiomyocytes from ischemia reperfusion injury via ROS and NO/ONOO-.
abstract: BACKGROUND
  Cardiac ischemia reperfusion (I/R) injury is associated with overproduction of reactive oxygen species (ROS). Low frequency pulse magnetic fields (LFMFs) have been reported to decrease ROS generation in endothelial cells. Whether LFMFs could assert protective effects on myocardial from I/R injury via ROS regulation remains unclear.
  
  
  METHODS
  To simulate in vivo cardiac I/R injury, neonatal rat cardiomyocytes were subjected to hypoxia reoxygenation (H/R) with or without exposure to LFMFs. Cell viability, apoptosis index, ROS generation (including O2(-) and ONOO(-)), and NO production were measured in control, H/R, and H/R + LFMF groups, respectively.
  
  
  RESULTS
  H/R injury resulted in cardiomyocytes apoptosis and decreased cell viability, whereas exposure to LFMFs before or after H/R injury significantly inhibited apoptosis and improved cell viability (P < 0.05). LFMFs treatment could suppress ROS (including O2(-) and ONOO(-)) generation induced by H/R injury, combined with decreased NADPH oxidase activity. In addition, LFMFs elevated NO production and enhanced NO/ONOO(-) balance in cardiomyocytes, and this protective effect was via the phosphorylation of endothelial nitric oxide synthase (eNOS).
  
  
  CONCLUSIONS
  LFMFs could protect myocardium against I/R injury via regulating ROS generation and NO/ONOO(-) balance. LFMFs treatment might serve as a promising strategy for cardiac I/R injury.
authors: Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shannxi 710032, China.
authors: Sai
authors: S
authors: Ma
authors: Zhengxun
authors: Z
authors: Zhang
authors: Fu
authors: F
authors: Yi
authors: Yabin
authors: Y
authors: Wang
authors: Xiaotian
authors: X
authors: Zhang
authors: Xiujuan
authors: X
authors: Li
authors: Yuan
authors: Y
authors: Yuan
authors: Feng
authors: F
authors: Cao
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002316:Cardiotonic Agents / Q000378:metabolism*; D015687:Cell Hypoxia / Q000187:drug effects; D002469:Cell Separation; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D060526:Magnetic Fields; D015428:Myocardial Reperfusion Injury / Q000201:enzymology / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000201:enzymology / Q000473:pathology*; D019255:NADPH Oxidases / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D010100:Oxygen / Q000494:pharmacology; D030421:Peroxynitrous Acid / Q000378:metabolism*; D010766:Phosphorylation / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D002316:Cardiotonic Agents; D017382:Reactive Oxygen Species; D030421:Peroxynitrous Acid; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D019255:NADPH Oxidases; D010100:Oxygen