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研究HL-60细胞在足叶乙甙（Vp16）诱导的细胞凋亡中bcl－2基因表达，以说明药物致调亡的分子机制。方法：采用细胞存活率，形态改变，DNA梯形片段分析和原位缺口标记法，分析药物引起的细胞凋亡，以细胞原位杂交和免疫组化分析bcl－2mRNA及其蛋白的表达水平。结果：Vp16有效地诱导HL60细胞凋亡，12h形成DNA缺口，16h出现DNA梯形片段，24h形成调亡小体，48hDNA完全降解；细胞凋亡时其bcl－2mRNA和蛋白水平都较处理前明显降低。结论:bcl－2基因表达的下调在Vp16诱导的HL-60细胞调亡中起一定作用。
To investigate the expression of bcl-2 gene in HL-60 cells induced by etoposide (Vp16) to illustrate the molecular mechanism of drug induced apoptosis. Methods: The cell apoptosis was analyzed by cell viability, morphological changes, DNA ladder analysis and in situ nick labeling. The expression of bcl-2 mRNA and protein was analyzed by in situ hybridization and immunohistochemistry. Results: Vp16 effectively induced apoptosis of HL60 cells, formed DNA gap at 12h, appeared DNA ladder fragment at 16h, formed apoptotic bodies at 24h and completely degraded at 48h. The mRNA and protein levels of bcl-2 were significantly lower than those before treatment . Conclusion: The down-regulation of bcl-2 gene expression may play a role in Vp16-induced apoptosis of HL-60 cells.