AIM:To investigate whether the chloride/bicarbonate (Cl-/HCO-3) exchanger is involved in staurosporine (STS) induced mouse cardiomyocyte apoptosis,and further understand the function of Cl-/HCO-3 exchanger in cell apoptosis. METHODS:To induce mouse cardiomyocyte apoptosis and to explore the effect of Cl-/HCO-3 exchanger,STS was used with two methods:⑴ different blocker,the chloride channel as well as exchanger blocker DIDS and the chloride channel blocker NPPB; ⑵ different culture medium with or without HCO-3 component. RESULTS:The cell viability and caspase-3 activity of DIDS and NPPB on STS-induced cardiomyocyte apoptosis were 59.7% and 47.2%,175.0% and 212.0% respectively with significant statistic differences (both P0.05,n=20). The cell viability and caspase-3 activity of STS-induced cardiomyocyte apoptosis in culture medium with or without HCO-3 were 29.8% and 41.6%,553.4% and 424.7%,respectively (both P

Objective To explore the role of potassium channel in cardiomyocyte apoptosis induced by ischemia/reperfusion process. Methods Cell viability,caspase-3 activity,intracellular reactive oxygen species(ROS)levels and cell membrane integrity were observed in apoptotic model of mouse cardiomyocytes induced by ischemia/reperfusion(I/R).Experiment groups included negative control,positive control(I/R)and drug treatment group(I/R + potassium channel blocker).Results (1)Potassium channel blockers potently inhibited cardiomyocyte apoptosis induced by I/R.Cell viability in Quinine(81.1%)and BaCl2(82.3%)groups were higher than in positive group (52.1%)(all P＜0.01).(2)Compared with positive control group(482.3%),potassium channel blockers(188.3% in Quinine group and 191.4% in BaCl2 group)inhibited caspase-3 activity significantly 24 hours after reperfusion(P＜0.01).(3)In both positive control and drug groups,the cell lactate dehydrogenase(LDH)leakage was less than 10% at 96 hours after reperfusion.Conclusions Potassium channel blockers can protect injured cardiomyocyte by inhibiting caspase-3 activity and ROS production in I/R process.