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目的：探讨粒－巨噬细胞集落刺激因子（ＧＭ－ＣＳＦ）对Ｖｐ１６诱导白血病细胞凋亡的调控作用，指导白血病临床治疗中正确使用ＧＭ－ＣＳＦ。方法：在构建高效表达ＧＭ－ＣＳＦ的逆转录载体Ｎ２Ａ／ＣＭＶ／ＧＭ－ＣＳＦ表达系统的基础上，对转ＧＭ－ＣＳＦ基因和未转ＧＭ－ＣＳＦ基因的白血病ＨＬ－６０细胞进行研究。结果：未转ＧＭ－ＣＳＦ基因及转空载体Ｎ２Ａ的ＨＬ－６０细胞经Ｖｐ１６处理后均出现凋亡的特征性表现：ＤＮＡ电泳呈梯状；流式细胞仪ＤＮＡ直方图上呈现特征性的亚二倍体（亚Ｇ１）峰；透射电镜观察细胞形态可见凋亡的特征性改变。结论：Ｖｐ１６具有诱导白血病细胞发生凋亡的作用，而ＧＭ－ＣＳＦ能够抑制Ｖｐ１６诱导的细胞凋亡。以上结果表明，白血病临床治疗中为预防和改善化疗所致骨髓抑制而应用ＧＭ－ＣＳＦ时，应谨慎地选择时机，在化疗前和化疗期间不宜使用，以避免白血病细胞对抗癌药物诱导的凋亡产生抵抗而导致耐药。
Objective: To investigate the regulation effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on apoptosis of leukemic cells induced by Vp16, and to guide the correct use of GM-CSF in clinical treatment of leukemia. METHODS: On the basis of constructing the N2A/CMV/GM-CSF expression system for GM-CSF expressing GM-CSF, the GM-CSF gene and GM-CSF-transgenic leukemic HL-60 cells were studied. RESULTS: The GM-CSF gene and HL-60 cells transfected with empty vector N2A exhibited apoptotic characteristics after Vp16 treatment: DNA electrophoresis was ladder-like; flow cytometry DNA histograms showed characteristic sub-patterns. Diploid (sub-G1) peaks; characteristic changes in apoptosis were observed by transmission electron microscopy. Conclusion: Vp16 can induce apoptosis of leukemia cells, while GM-CSF can inhibit Vp16-induced apoptosis. The above results indicate that when clinically treating leukemia with GM-CSF for preventing and improving myelosuppression caused by chemotherapy, the timing should be carefully chosen, and it should not be used before or during chemotherapy to prevent leukemia cells from being induced by anticancer drugs. Death caused resistance and led to drug resistance.