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目的 探讨Ａｒａ－Ｃ及ＶＭ２６治疗白血病的机制。方法 应用细胞形态学检查、二苯胺法ＤＮＡ片段化定量及ＤＮＡ 凝胶电泳方法研究阿糖胞苷（Ａｒａ－Ｃ）、ＶＭ２６诱导原代培养的急性非淋巴细胞白血病（ＡＮＬＬ）细胞凋亡结果 原代培养的ＡＮＬＬ细胞体外孵育２４ ｈ，空白组细胞ＤＮＡ 片段率仅为（１５．１±３．３）％ ，加Ａｒａ－Ｃ５０ μｇ／Ｌ组和ＶＭ２６ １０ ｍ ｇ／Ｌ，ＤＮＡ片段率均显著增高，分别达（４１．８±１９．１）％ 和（４６．８±１８．７）％ （Ｐ＜ ０．０１，ｎ＝ １１）。两种药物诱导ＤＮＡ片段化均呈剂量和时间依赖性。光镜下见两种药物均诱导ＡＮＬＬ细胞出现典型的细胞凋亡形态改变。ＤＮＡ 电泳显示典型的ＤＮＡ Ｌａｄｄｅｒ。结论 Ａｒａ－Ｃ及ＶＭ２６ 能诱导ＡＮＬＬ细胞出现凋亡，诱导白血病细胞凋亡可能是其抗白血病作用的主要机制之一。
Objective To investigate the mechanism of Ara-C and VM26 in the treatment of leukemia. METHODS: Apoptosis of primary non-lymphoblastic leukemia (ANLL) cells induced by Ara-C and VM26 was studied by using cell morphology, DNA fragmentation quantification and DNA gel electrophoresis. The cultured ANLL cells were incubated in vitro for 24 h. The blank cell DNA fragment ratio was only (15.1±3.3)%. The Ara-C50 μg/L group and VM26 10 m g/L showed significant DNA fragmentation rates. The increase was (41.8±19.1)% and (46.8±18.7)%, respectively (P<0.01, n=11). Both drugs induce DNA fragmentation in a dose- and time-dependent manner. Under light microscope, both drugs induced the typical apoptosis morphology of ANLL cells. DNA electrophoresis shows a typical DNA Ladder. Conclusion Ara-C and VM26 can induce apoptosis in ANLL cells. Inducing apoptosis of leukemia cells may be one of the main mechanisms of anti-leukemia effect.