【摘要】 目的　深入了解异搏定 (verapamil,VER)对鬼臼乙叉甙 (etoposide,VP1 6)增敏作用的机制。方法　以人急性髓性白血病细胞株 HL- 60为研究对象 ,运用 DNA电泳、流式细胞仪 (flow cytom etry,FCM)两种方法观察细胞凋亡现象 ,用 Western blotting方法测定凋亡相关蛋白 bcl- 2表达水平。结果　 5 m g/ L VER可增强 VP1 6的诱导细胞凋亡作用 ,并可下调 bcl- 2蛋白表达水平。结论　 VER对 VP1 6具有增敏作用与其具有增强 VP1 6诱导 HL- 60细胞凋亡作用有关 ;Bcl- 2蛋白可能是这一作用的靶点。更多还原

【Abstract】 Objective To study the possible mechanisms of verapamil enhance the antitumor activity of etoposide.Methods Modulation of etoposide induced apoptosis by verapamil in HL 60 cells was studied by DNA fragmentation、Flow cytometry(FCM) and Western blotting.Verapamil exhibited a 7.4 foid potentiation on apoptosis caused by etoposide in HL 60 cells for a 8h exposure.Results Etoposide induced apoptosis and its potentiation by verapamil were associated with reduced bcl 2 expression.Conclusion Our data suggest that verapamil may enhance the antitumor activity of etoposide through potentiate the apoptosis induced by etoposide,and implicated bcl 2 may play a role in this pathway.更多还原