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目的 :探讨 topo 抑制剂的抗瘤机制。方法 :选择人急性早幼粒细胞白血病细胞株 HL- 60为实验模型 ,以 VP- 1 6为诱导剂 ,用形态学观察、DNA电泳及流式细胞术 ( FCM)等方法对其凋亡情况进行了研究。 结果 :经 VP- 1 6处理的 HL- 60细胞呈典型凋亡形态学改变 ,出现梯状 DNA条带 ( DNA ladder) ,FCM DNA直方图上 G0 /G1峰前有明显的亚二倍体凋亡峰。表明经 VP- 1 6处理的 HL- 60细胞的确发生了凋亡 ,这种调亡作用对药物有浓度依赖性 ,但无严格时间依赖性 ,不需药物的持续作用 ,并与 S期细胞降低有关。而缺乏 topo 的 HPBL则无此作用 ,不受 VP- 1 6诱导而凋亡。结论 :诱导细胞凋亡是 VP- 1 6的抗瘤机制之一 ,且这种作用是由 topo 介导的。
Objective: To investigate the anti-tumor mechanism of topo inhibitor. Methods: Human acute promyelocytic leukemia cell line HL-60 was selected as experimental model and VP-1 6 as inducer. Morphological observation, DNA electrophoresis and flow cytometry (FCM) Were studied. Results: HL-60 cells treated with VP-1 6 showed typical morphological changes of apoptosis. DNA ladders appeared. The sub-diploid was observed before G0 / G1 peak on the FCM DNA histogram Peak. This indicates that apoptosis of HL-60 cells treated with VP-1 6 did occur in a concentration-dependent manner but not in a time-dependent manner, without a sustained effect of the drug and decreased with S phase cells related. However, HPBL lacking topo had no effect and was not induced by VP-1 6 and apoptosis. CONCLUSION: Induction of apoptosis is one of the anti-tumor mechanisms of VP-1 6, and this effect is mediated by topo.