阿糖胞苷诱导HL—60细胞凋亡的研究

明确化疗药物诱导急性白血病细胞凋亡的规律及在急性白血病化疗中的意义。方法应用光镜、电镜,结合ＤＮＡ电泳及流式细胞仪分析技术,观察阿糖胞苷（Ａｒａ－ｃ）诱导的急性髓系白血病细胞系ＨＬ－６０凋亡模式。结果Ａｒａ－ｃ诱导的细胞凋亡在０～３６小时过程中持续存在,逐渐增强,其诱导效率呈剂量性增强。而且,经其他６种化疗药物诱导后,ＨＬ－６０以及经ＤＡ方案化疗的１例急性髓系白血病患者外周血白细胞,均表现典型的ＤＮＡ梯形图谱。进一步分析表明,化疗诱导凋亡与其下调ｃ－ｍｙｃ、ｂｃｌ－２基因表达有关。结论化疗药物诱导的细胞凋亡是化疗的关键机制

Ara-c induced apoptosis in human myeloid leukemia cell line HL-60

Objective To elucidate the pattern of chemotherapy drugs induced apoptosis and its role in chemotherapy of acute leukemia. Methods Apoptosis induced by Ara c in human myeloid leukemia cell line HL 60 was investigated by applying light microscopy, electron microscopy combined with DNA electrophoresis and flow cytometry analysis techniques. Results Apoptosis persisted throughout 36 hours following addition of Ara c with a gradual augmentation. Efficiency of apoptosis was enhanced in a dose dependent pattern, HL 60 treated with six other chemotherapy drugs and perpherial white blood cells from a AML case undergoing DA protocol chemotherapy exhibited typical DNA ladder pattern. Further investigation indicated that chemotherapy drugs induced apoptosis came into being possibly by downregulation the oncogenes expression of c myc and bcl 2. Conclusion Chemotherapy induced apoptosis is a primary mechanism in chemotherapy.