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Proteomics Research on the Protective Effect of Mangiferin on H9C2 Cell Injury Induced by H2O2
Wei Guan1, Yan Liu2, Yuan Liu2
1Key Laboratory of Chinese Materia Medica, Ministry of Education of Heilongjiang University of Chinese Medicine, Harbin 150040, China. myguanwei1234@yeah.net.
Insights
Mangiferin protects heart cells from injury by boosting antioxidant capacity and improving energy metabolism pathways. This natural compound offers a promising therapeutic avenue for cardiovascular disease, specifically myocardial ischemia reperfusion injury (MIRI).
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Cardiovascular diseases represent a significant global health burden, causing widespread morbidity and mortality.
- Mangiferin, a natural glucosylxanthone, exhibits antioxidant and anti-inflammatory properties, suggesting cardioprotective potential.
- The precise molecular mechanisms underlying mangiferin's protection against myocardial ischemia reperfusion injury (MIRI) remain largely unexplored.
Purpose of the Study:
- To investigate the protective effects of mangiferin against MIRI using an in vitro H9C2 cell injury model.
- To elucidate the underlying molecular mechanisms of mangiferin's cardioprotection via isobaric tags for relative and absolute quantitation (iTRAQ)-based proteomics.
Main Methods:
- An in vitro model of MIRI was established using H9C2 cells subjected to hydrogen peroxide (H2O2)-induced injury.
- The protective effects of mangiferin were assessed by measuring its impact on oxidative stress and cell viability.
- iTRAQ-based proteomics was employed to identify differentially expressed proteins and explore molecular pathways affected by mangiferin.
Main Results:
- Mangiferin significantly improved the antioxidant capacity of H9C2 cells, mitigating oxidative imbalance.
- Proteomics analysis identified twenty proteins that were normalized by mangiferin pretreatment, primarily involved in glucose and fatty acid metabolism.
- Kyoto Encyclopedia of Gene and Genomes (KEGG) analysis highlighted the activation of glycolysis, the citrate cycle, and fatty acid degradation pathways.
- Western blot validation confirmed the proteomic findings for six key cardiac metabolism-related proteins.
Conclusions:
- Mangiferin demonstrates significant cardioprotective effects against MIRI by enhancing cellular antioxidant capacity.
- Mangiferin promotes cardiomyocyte survival by upregulating key metabolic pathways, including glycolysis, the citrate cycle, and fatty acid degradation.
- These findings highlight mangiferin as a potential therapeutic agent for managing MIRI and related cardiovascular conditions.
Abstract:
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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