Roles of CFTR Cl- channels in hydrogen sulfide-induced cardioprotection and cell proliferation in H9c2 cells

AIM: To explore the roles of cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels in hydrogen sulfide (H2S)-induced cardioprotection and cell proliferation in H9c2 cells. METHODS: Cobalt chloride (CoCl2) was used to set up the chemical hypoxia-induced injury model in H9c2 cells. Myocardial cell viability was detected by the CCK-8 assay kit. Apoptotic changes in H9c2 cells were observed by using Hoechst 33342 staining and photofluorography. RESULTS: At the concentrations from 400 to 2 000 μmol/L, CoCl2 dose-dependently inhibited cell viability in H9c2 cells. CoCl2 at concentration of 600 μmol/L significantly induced H9c2 cell apoptosis. Sodium hydrosulfide (NaHS) at concentrations from 100 to 400 μmol/L dose-dependently enhanced proliferation in H9c2 cells. NaHS protected H9c2 cells against CoCl2-induced injury, including an increase in cell viability and a decrease in percentage of apoptosis. 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB, 100 μmol/L), an inhibitor of CFTR Cl- channels alone did not damaged H9c2 cells, but considerably blocked the inhibitory effect of NaHS on CoCl2 cytotoxicity. However, NPPB did not antagonize the NaHS-induced antiapoptotic effect and cell proliferation in H9c2 cells. CONCLUSION: CFTR Cl- channels may be involved in the inhibitory effect of H2S on CoCl2-induced cytotoxicity in H9c2 cells.