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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Westernblotting方法测定凋亡相关蛋白BCL 2表达水平。结果 :在作用 2 0h后 ,5mg·L-1VER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: To understand the mechanism of reversal of resistance to etoposide (VP16) by verapamil (VER). Methods: HL-60 / ADR cells were stained with multidrug resistance-associated protein (MRP), and cell apoptosis was detected by DNA electrophoresis and flow cytometry. Western blotting Methods The expression of apoptosis related protein BCL 2 was measured. Results: After treated with 5 mg · L-1VER for 20 h, VP16 could enhance the apoptosis induced by HL 60 / ADR by 2.8 times and decrease the expression of BCL 2 protein. CONCLUSION: The reversal effect of VER on VP16 may be related to its effect on enhancing the apoptosis of HL-60 cells induced by VP16. BCL-2 protein may be the target of this action