足叶乙甙诱导HL-60细胞凋亡及其bcl-2基因表达  

THE EXPRESSION OF BCL-2 GENE DURING APOPTOSIS OF HL-60 CELLS INDUCED BY ETOPSIDE

作　　者：张萍[1] 郝红樱[2] 王申五[1] 张翼军[3] 陆道培[1] 

机构地区：[1]北京医科大学人民医院血液病研究所,100034 [2]北京武警总医院 [3]第三军医大学附属西南医院

出　　处：《北京医科大学学报》1997年第5期403-405,共3页Journal of Peking University(Health Sciences)

基　　金：国家自然科学基金!39470316

摘　　要：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。Objective: To study bcl-2 gene expression in HL-60 cell apoptosis induced by etopside and show the biologic mechanism of apoptosis induced by drugs. Methods: Cell survival rate, cell morphologic changes,DNA ladder analysis and DNA nick end labelling in situ methods were used to analyze cell apoptoois induced by etopside. Cell hybridization in situ and immunohistochemistry were used to analyze bcl- 2 mRNA a nd bcl - 2protein expression. Results: Vp16 can induce HL-60 cell apoptosis effectively, DNA nick was formed after 12hours DNA ladder was formed after 16 hours, apoptosis body was formed after 24 hours, DNA was completely degraded after 48 hours, bcL-2 mRNA and protein levels all reduced after being treated by Vp16.Conclusion: The reduction of bcL-2 gene expression played an important role in HL-60 cell apoptosis induced by etopside.

关 键 词：HL-60细胞 基因表达 细胞凋亡 足叶乙甙 BCL-2 

分 类 号：R329.5[医药卫生—人体解剖和组织胚胎学]