Role of potassium and chloride channel blockers in apoptosis of cardiomyocytes induced by staurosporine

    WANG Xiaoª²Ming, ZANG Yiª²Min£¬GONG Weiª²Qin£¬GAO Feng, LI Yuan, TAKAHASHI Nobuyuki, OKADA Yasunobu

    1Department of Geriatrics, Xijing Hospital, 2Department of Physiology, School of Basic Medicine, Fourth Military Medical University, Xi¡¯an 710033, China, 3Department of Cell Physiology, National Institute for Physiological Sciences, Okazaki 4448585, Japan

    ¡¾Abstract¡¿ AIM: To explore the role of potassium and chloride channel blockers in cardiomyocyte apoptosis process and their relationship with caspaseª²3 activation. METHODS: Primarily cultured mouse cardiomyocytes were exposed to staurosporine and the cell viability, DNA fragmentations, caspaseª²3 activation, and cell membrane integrity were observed in three groups: Normal control (without treatment), positive control (staurosporine) and drug group (staurosporine + potassium or chloride channel blocker). RESULTS: ¢Ù Potassium and chloride channel blockers potently inhibited cardiomyocytes apoptosis induced by staurosporine. Compared to the positive control group, the cell viability in drug group increased significantly (P<0.01) but apoptotic DNA fragmentations were suppressed in cardiomyocytes apoptosis induced by staurosporine. ¢Ú Potassium and chloride channel blockers also remarkably inhibited caspaseª²3 activity activated by staurosporine. Compared to the positive control group, caspaseª²3 activation decreased significantly (P<0.01) in drug group. ¢Û In both positive control and drug groups, the cell lactate dehydrogenase (LDH) leakage was less than 10%. CONCLUSION: Potassium and chloride channel blockers can remarkably inhibit cardiomyocytes apoptosis mediated by caspaseª²3 activation in the model of mouse cardiomyocyte apoptosis induced by staurosporine. ......