title: Levocarnitine protects H9c2 rat cardiomyocytes from H2O2-induced mitochondrial dysfunction and apoptosis.
abstract: BACKGROUND
  Although the protective effects of levocarnitine in patients with ischemic heart disease are related to the attenuation of oxidative stress injury, the exact mechanisms involved have yet to be fully understood. Our aim was to investigate the potential protective effects of levocarnitine pretreatment against oxidative stress in rat H9c2 cardiomyocytes.
  
  
  METHODS
  Cardiomyocytes were exposed to H2O2 to create an oxidative stress model. The cells were pretreated with 50, 100, or 200 μM levocarnitine for 1 hour before H2O2 exposure.
  
  
  RESULTS
  H2O2 exposure led to significant activation of oxidative stress in the cells, characterized by reduced viability, increased intracellular reactive oxygen species, lipid peroxidation, and reduced intracellular antioxidant activity. Mitochondrial dysfunction was also observed following H2O2 exposure, reflected by the loss of mitochondrial transmembrane potential and intracellular adenosine triphosphate. These pathophysiological processes led to cardiomyocyte apoptosis through activation of the intrinsic apoptotic pathway. More importantly, the levocarnitine pretreatment attenuated the H2O2-induced oxidative injury significantly, preserved mitochondrial function, and partially prevented cardiomyocyte apoptosis during the oxidative stress reaction. Western blotting analyses suggested that levocarnitine pretreatment increased plasma protein levels of Bcl-2, reduced Bax, and attenuated cytochrome C leakage from the mitochondria in the cells.
  
  
  CONCLUSIONS
  Our in vitro study indicated that levocarnitine pretreatment may protect cardiomyocytes from oxidative stress-related damage.
authors.affiliation: 1. Department of Cardiology, China-Japan Union Hospital, Jilin University, Changchun, China;
authors.forename: Cui-Ying
authors.initials: CY
authors.lastname: Mao
authors.affiliation: 2. College of Pharmacy, Jilin University, Changchun, China.
authors.forename: Hai-Bin
authors.initials: HB
authors.lastname: Lu
authors.affiliation: 2. College of Pharmacy, Jilin University, Changchun, China.
authors.forename: Ning
authors.initials: N
authors.lastname: Kong
authors.affiliation: 1. Department of Cardiology, China-Japan Union Hospital, Jilin University, Changchun, China;
authors.forename: Jia-Yu
authors.initials: JY
authors.lastname: Li
authors.affiliation: 1. Department of Cardiology, China-Japan Union Hospital, Jilin University, Changchun, China;
authors.forename: Miao
authors.initials: M
authors.lastname: Liu
authors.affiliation: 1. Department of Cardiology, China-Japan Union Hospital, Jilin University, Changchun, China;
authors.forename: Chun-Yan
authors.initials: CY
authors.lastname: Yang
authors.affiliation: 1. Department of Cardiology, China-Japan Union Hospital, Jilin University, Changchun, China;
authors.forename: Ping
authors.initials: P
authors.lastname: Yang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002331:Carnitine / Q000494:pharmacology*; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D008928:Mitochondria / Q000187:drug effects*; D032383:Myocytes, Cardiac / Q000187:drug effects*; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats
chemical_list: D006861:Hydrogen Peroxide; D002331:Carnitine
keywords: Apoptosis; Ischemic heart disease.; Levocarnitine; Mitochondrial dysfunction; Oxidative stress