Abstract: | AIM: To investigate the roles of ATP-sensitive potassium (KATP) channels in high glucose-induced cardiac injury and the inhibitory effect of hydrogen sulfide (H2S) on the cardiomyocyte injury. METHODS: The expression level of KATP channel protein was tested by Western blot. The cell viability was measured by CCK-8 assay. The number of apoptotic cells was observed by Hoechst 33258 nuclear staining. Mitochondrial membrane potential (MMP) was examined by JC-1 staining. RESULTS: After the H9c2 cells were treated with 35 mmol/L glucose (high glucose, HG) for 1~24 h, the protein level of KATP channel was significantly reduced at 6 h, 9 h, 12 h and 24 h, reaching the minimum level at 12 h and 24 h. Pretreatment of the cells with 400 μmol/L NaHS (a donor of H2S) prior to exposure to HG for 12 h considerably blocked the down-regulation of KATP channels induced by HG. Pretreatment of the cells with 100 μmol/L mitochondrial KATP channel opener diazoxide, 50 μmol/L non-selective KATP channel opener pinacidil or NaHS obviously inhibited HG-induced injuries, leading to an increase in the cell viability, and decreases in the number of apoptotic cells and the MMP loss. Pretreatment with 100 μmol/L mitochondrial KATP channel antagonist 5-hydroxydecanoic acid or 1 mmol/L non-selective KATP channel antagonist glibenclamide attenuated the above cardioprotective effects of NaHS. CONCLUSION: KATP channels mediate the inhibitory effect of H2S on HG-induced cardiac injury. |