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.
Keywords: apoptosis; cardiomyocyte; high glucose; hydrogen sulfide; oxidative stress.