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作 者:陈丽娟[1] 李建勇[1] 钱思轩[1] 朱广荣[1] 郑文娟[1]
机构地区:[1]南京医科大学第一附属医院,江苏省人民医院血液科,南京210029
出 处:《中国实验血液学杂志》2006年第4期696-699,共4页Journal of Experimental Hematology
基 金:江苏省社会发展计划基金(编号BS2006071);江苏省135工程医学重点人才基金资助项目(编号RC2002044);江苏省人民医院人才启动基金资助项目(编号155NA0505)
摘 要:为了研究velcade诱导多发性骨髓瘤细胞株U266细胞凋亡效应及机制,采用台盼蓝拒染法检测2、10、50和100nmol/Lvelcade处理U266细胞活率,用流式细胞术分析Annexin-V、线粒体跨膜电位(Δψm)和氧自由基(ROS),用半定量RT-PCR法检测bcl-2mRNA的表达。结果表明velcade抑制U266细胞增殖;诱导U266细胞凋亡,24小时Annexin-V阳性细胞比例增高,△ψM降低;12小时时活性氧明显增高,荧光强度增强;抗凋亡基因bcl-2表达降低。结论velcade对U266细胞具有增殖抑制和杀伤作用,其可通过内源性细胞凋亡信号通路诱导U266细胞凋亡。To investigate the effect of velcade on multiple myeloma cell line U266 apoptosis and its mechanism, cell viability was estimated by trypan blue dye exclusion. Annexin-V, mitochondrial transmembrane potential (△ψm) and reactive oxygen species (ROS) labeled by DCFHDA were examined by flow cytometry, the expression of bcl-2 mRNA was detected by semi-quatitafive RT-PCR. The results showed that the velcade inhibited the growth of U266 cells and reduced cell viability accompanied by appearance of morphologic characteristics of apoptosis. Velcade at 50 nmol/L increased Annexin V positivity and fluorescence intensity of DCF because of ROS generation while it decreased the △ψm of U266 cells. Expression of anti-apoptotic gene bcl-2 mRNA also decreased. It is concluded that velcade inhibite the growth and reduce cell viability of U266 cells. Velcade can induce U266 cells apoptosis by intrinsic cell apoptotic pathway.
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