4.6 Article

Proteomics Research on the Protective Effect of Mangiferin on H9C2 Cell Injury Induced by H2O2

期刊

MOLECULES
卷 24, 期 10, 页码 -

出版社

MDPI
DOI: 10.3390/molecules24101911

关键词

iTRAQ; proteomics; mangiferin; H9C2; oxidative stress; myocardial ischemia and reperfusion injury

资金

  1. National key basic research development program (973 Program) of China [2013CB531801]
  2. University Nursing Program for Yong Scholars with Creative Talents in Heilongjiang Province [UNPYSCT-2017221]
  3. Natural Science Foundation of Heilongjiang Province of China [YQ2019H029]

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Cardiovascular disease is one of the leading causes of morbidity and mortality worldwide. Mangiferin is a natural glucosylxanthone with antioxidant and anti-inflammatory properties, which has been confirmed to protect cardiac cells from myocardial infarction and myocardial ischemia reperfusion injury (MIRI); however, the underlying mechanism is still unclear. As oxidative stress is a major pathogenesis of MIRI, an H9C2 cell injury induced by hydrogen peroxide (H2O2) was established to simulate MIRI in vitro. Herein, the protective effect of mangiferin against MIRI was evaluated and the isobaric tags for relative and absolute quantitation (iTRAQ)-based proteomics was applied to explore the underlying molecular mechanism. In this research, mangiferin markedly ameliorated the oxidative imbalance by increasing the antioxidative capacity of the H9C2 cell. Moreover, proteomics analysis revealed that mangiferin pretreatment brought twenty differently-expressed proteins back to normal, most of which were related to glucose and fatty acid metabolism. Glycolysis, citrate cycle, and fatty acid degradation pathways were highlighted by Kyoto Encyclopedia of Gene and Genomes (KEGG) analysis. Western blot validation of six cardiac metabolism-related proteins were consistent with the proteomics analysis. Taken together, mangiferin protected the cardiomyocytes from MIRI by enhancing the antioxidant capacity and increasing the activities of glycolysis, citrate cycle, and fatty acid degradation pathways.

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