异搏定逆转HL-60/ADR细胞株耐药机理的初步探讨-东南大学学报医学版

异搏定逆转HL-60/ADR细胞株耐药机理的初步探讨

单位：1.南京铁道医学院附属医院,血液科,江苏,南京,210009； 2.南京军事医学研究所,防护室,江苏,南京,210002

分类号：R972, R733.71, R329.2

出版年·卷·期（页码）：2000·19·第一期（11-13）

摘要：

目的:深入了解异搏定(VER)对鬼臼乙叉甙(VP16)耐药逆转作用的机制.方法:以多药耐药相关蛋白(MRP)高表达的耐阿霉素人急性髓性白血病细胞株HL-60/ADR为研究对象,应用DNA电泳、流式细胞仪观测细胞凋亡现象,用Western blotting方法测定凋亡相关蛋白BCL-2表达水平.结果:在作用20h后,5mg.L-1 VER可使VP16对HL-60/ADR诱导凋亡作用增强2.8倍,并可下调BCL-2蛋白表达水平.结论:VER对VP16的耐药逆转作用可能与其具有增强VP16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.

Objective The experiment was designed to study the possible mechanisms of verapamil in reversal effect on HL?60/ADR cells.Methods Modulation of etoposide?induced apoptosis by verapamil in HL?60/ADR cells was studied by DNA fragmentation,Flow cytometry(FCM) and Western blotting.Results Verapamil exhibited 2.8 fold potentiation on apoptosis caused by etoposide in HL?60/ADR cells for 20?h exposure.Etoposide?induced apoptosis and its potentiation by verapamil were associated with reduced BCL?2 expression.Conclusion Our data suggest that the reversal effect of verapamil on VP16 may be assciated with its enhancement of VP16 in inducing HL?60 apoptosis,and the BCL?2 may play a role in this pathway.

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