ETHNOPHARMACOLOGICAL RELEVANCE: Musk has been traditionally used in Chinese medicine as the main ingredient of many formulations for the treatment of chest pain and angina pectoris. AIM OF THE STUDY: 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. MATERIALS AND 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. CONCLUSION: 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. Copyright Â
ETHNOPHARMACOLOGICAL RELEVANCE: Musk has been traditionally used in Chinese medicine as the main ingredient of many formulations for the treatment of chest pain and angina pectoris. AIM OF THE STUDY: 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. MATERIALS AND 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. CONCLUSION: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. Copyright Â