title: Protective effects of muscone on ischemia-reperfusion injury in cardiac myocytes.
abstract: BACKGROUND
  Musk has been traditionally used in Chinese medicine as the main ingredient of many formulations for the treatment of chest pain and angina pectoris.
  
  
  OBJECTIVE
  To investigate the protective effects of muscone (the active ingredient of musk) on ischemia-reperfusion (I/R) injury induced by hypoxia and low glucose in primary cultured rat cardiac myocytes.
  
  
  METHODS
  Primary cultures of neonatal rat cardiac myocytes were subjected to ischemia-reperfusion in media, with or without muscone. Cell viability, release of lactic acid dehydrogenase (LDH), superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, creatine kinase (CK) and caspase-3 activities, as well as intracellular free Ca(2+) concentrations, were measured. Cellular apoptosis and mitochondrial membrane potential (MMP) were assessed by flow cytometry, and the expression of Bcl-2 and Bax proteins was assessed by Western blotting.
  
  
  RESULTS
  Following the exposure of cardiac myocytes to ischemia-reperfusion, there was a marked decrease in pulsating frequency, cell viability, SOD activity, MMP, and the expression of Bcl-2 protein, accompanied by increased LDH release, MDA production, CK and caspase-3 activities, intracellular free Ca(2+) concentrations, rate of apoptosis, and expression of Bax protein. Pretreatment with muscone (0.215, 0.43, 0.86 μg/mL) prior to I/R injury significantly attenuated the above changes.
  
  
  CONCLUSIONS
  Muscone has a protective effect against I/R injury in cardiac myocytes, indicating that muscone may potentially provide therapeutic benefit in I/R injury by inhibiting cellular oxidative stress and apoptosis.
authors.affiliation: Faculty of Chinese Medicine, Macau University of Science and Technology, Macau 999078, China. qbwu@must.edu.mo
authors.forename: Qibiao
authors.initials: Q
authors.lastname: Wu
authors.forename: Haitao
authors.initials: H
authors.lastname: Li
authors.forename: Ye
authors.initials: Y
authors.lastname: Wu
authors.forename: Weixing
authors.initials: W
authors.lastname: Shen
authors.forename: Li
authors.initials: L
authors.lastname: Zeng
authors.forename: Haibo
authors.initials: H
authors.lastname: Cheng
authors.forename: Ling
authors.initials: L
authors.lastname: He
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D001188:Artiodactyla; D002118:Calcium / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D003402:Creatine Kinase / Q000378:metabolism; D003516:Cycloparaffins / Q000494:pharmacology / Q000627:therapeutic use*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000975:Antioxidants; D003516:Cycloparaffins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D008315:Malondialdehyde; D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase; D003402:Creatine Kinase; D053148:Caspase 3; D002118:Calcium; C031021:muscone