Hydrogen sulfide inhibits high-glucose-induced apoptosis in neonatal rat cardiomyocytes

Abstract

Hydrogen sulfide (H₂S), an endogenous signaling molecule with potent cytoprotective effects, has been shown to provide cardioprotection in various models of cardiac injury. The present study was designed to investigate the protective effects of H₂S against high-glucose-induced cardiomyocyte apoptosis and explore the potential mechanisms using cultured neonatal rat cardiomyocytes. The apoptotic rate of cardiomyocytes was determined by flow cytometry with Annexin V/propidium iodide staining. Oxidative stress was evaluated by detecting concentration of malondialdehyde and superoxide dismutase in the supernatant of culture media. The mRNA and protein expression of Bax and Bcl-2 was determined by realtime PCR and Western blotting. Our findings suggested that H₂S could protect against cardiomyocyte apoptosis induced by high glucose. Moreover, H₂S was also found to reduce high-glucose-induced oxidative stress and alter the mRNA and protein expression of Bax and Bcl-2. In conclusion, our study demonstrates that H₂S protects against high-glucose-induced cardiomyocyte apoptosis by attenuating oxidative stress and altering apoptosis regulatory gene expression.