title: H2O2 evokes injury of cardiomyocytes through upregulating HMGB1.
abstract: BACKGROUND
  Reactive oxygen species (ROS) have been shown to induce cell apoptosis in cardiomyocytes. However, the underlying mechanism remains unclear. This study aimed to investigate the role of high-mobility group box 1 protein (HMGB1) in cardiomyocytes undergoing H2O2 treatment.
  
  
  METHODS
  Neonatal rat cardiomyocytes were treated with H2O2 (100, 200, 500 µM) or pre-treated with antioxidant N-acetylcysteine (NAC 200 µM) or HMGB1 neutralizing antibody (20 µg/ml) in an appropriate concentration of H2O2 (200 µM). The cell viability, apoptosis rate, lactate dehydrogenase (LDH), and the activity of superoxide dismutase were measured. HMGB1 expression was assessed by immunoblotting.
  
  
  RESULTS
  H2O2-induced ROS significantly decreased cell viability, promoted the apoptosis of neonatal myocytes, and upregulated the expression of HMGB1 in a dose-dependent manner. However, NAC or HMGB1 neutralizing antibody suppressed the loss of cell viability and the rate of cell apoptosis induced by H2O2. NAC or HMGB1 neutralizing antibody also significantly suppressed the release of LDH and the expression of HMGB1.
  
  
  CONCLUSIONS
  The present study suggests that H2O2-induced ROS evoke injury to cardiomyocytes that may be associated with upregulating HMGB1.
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University; Cardiovascular Research Institute of Wuhan University, Wuhan, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Xie
authors.forename: Xiaoya
authors.initials: X
authors.lastname: Zhou
authors.forename: Xiaorong
authors.initials: X
authors.lastname: Hu
authors.forename: Hong
authors.initials: H
authors.lastname: Jiang
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D000818:Animals; D057134:Antibodies, Neutralizing / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D002316:Cardiotonic Agents / Q000378:metabolism / Q000494:pharmacology; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D024243:HMGB1 Protein / Q000378:metabolism*; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D057134:Antibodies, Neutralizing; D000975:Antioxidants; D002316:Cardiotonic Agents; D024243:HMGB1 Protein; C104200:Hbp1 protein, rat; D017382:Reactive Oxygen Species; D006861:Hydrogen Peroxide; D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase; D000111:Acetylcysteine