期刊
NITRIC OXIDE-BIOLOGY AND CHEMISTRY
卷 46, 期 -, 页码 114-122出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.niox.2014.12.007
关键词
Hydrogen sulfide; Cardiac hypertrophy; Glucose transporter
资金
- key laboratory program of the Shanghai Municipal Education Commission [ZDSYS14005]
Introduction: Hydrogen sulfide (H2S) has been reported to inhibit myocardial hypertrophy in a cell model of cardiomyocyte hypertrophy. Our previous study also shows an H2S-induced increase in glucose metabolism in insulin-targeting cells. The present study aims to examine the hypothesis that H2S attenuates myocardial hypertrophy and promotes glucose utilization in cardiomyocytes. Methods: The cell model of cardiomyocyte hypertrophy was induced by application of phenylephrine and cardiomyocyte hypertrophy was examined using leucine incorporation assay. Protein levels were measured using Western blot analysis. The activity of related enzymes was measured with enzyme-linked immunosorbent assay (ELISA). Results: NaHS (an H2S donor) treatment increased the activity of cultured cardiomyocytes and reduced hypertrophy in cultured cardiomyocytes at concentrations ranging from 25 to 200 mu mol/L. NaHS treatment increased glucose uptake and the efficiency of glycolysis and the citric acid cycle. The key enzymes in these reactions, including lactate dehydrogenase and pyruvate kinase and succinate dehydrogenase, were activated by NaHS treatment (100 mu mol/L). Some intermediates of glycolysis and the citric acid cycle, including lactic acid, cyclohexylammonium, oxaloacetic acid, succinate, L-dimalate, sodium citrate, cis-aconitic acid, ketoglutarate and DL-isocitric acid trisodium also showed anti-hypertrophic effects in cardiomyocytes. Conclusions: H2S improves glucose utilization and inhibits cardiomyocyte hypertrophy. (C) 2014 Elsevier Inc. All rights reserved.
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