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Protective effects of muscone on ischemia-reperfusion injury in cardiac myocytes
Authors:Wu Qibiao  Li Haitao  Wu Ye  Shen Weixing  Zeng Li  Cheng Haibo  He Ling
Institution:a Faculty of Chinese Medicine, Macau University of Science and Technology, Macau 999078, China
b Department of Pharmacology, Nanjing University of Chinese Medicine, Nanjing 210009, China
c China Pharmaceutical University, Nanjing 210009, China
Abstract:

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 Ca2+ 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 Ca2+ 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.
Keywords:I/R  ischemia-reperfusion  LDH  lactic acid dehydrogenase  SOD  superoxide dismutase  MDA  malondialdehyde  CK  creatine kinase  MMP  mitochondrial membrane potential
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