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抑制NF-κB通路增强蟾蜍灵诱导的HL-60细胞凋亡 被引量:4

Blockage of NF-κB pathway enhanced bufalin-induced HL-60 cell apoptosis
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摘要 目的:观察蟾蜍灵对HL-60细胞活力和凋亡的影响,对NF-κB通路的作用,探讨NF-κB通路在蟾蜍灵诱导HL-60细胞凋亡过程中的作用。方法:锥虫蓝染色检测细胞活力;流式细胞仪技术检测细胞凋亡和周期分布;采用WesternBlot技术检测IKK的磷酸化。结果:蟾蜍灵以时间和剂量依赖性方式诱导HL-60细胞凋亡。24,48和72h抑制细胞活力的IC50浓度分别为26.3,7.8和2.0nmol/L。对照组HL-60细胞有pIKK表达,蟾蜍灵可诱导IKK的快速活化。NF-κB通路的特异性抑制剂Bay11-7082增强蟾蜍灵的凋亡诱导作用。结论:蟾蜍灵可诱导HL-60细胞凋亡,促进IKK活化与NF-κB通路调节相关,而且与NF-κB通路抑制剂有协同作用。 Objective :To investigate the effects of bufalin on HL- 60 cell viability, apoptosis and NF- κB path- way activation, nehtods:Cell viability was tested by Trypan Blue Staining. Apoptosis was detected using flow cytometery assay. The expressions of pIKK and IKK were tested by using Western Blot. Results: Bufalin inhibited HL - 60 cell viability in a time - and dose - dependent manner. Concentrations of bufalin that inhibited 50% cell viability (IC50) for 24h,48h and 72h were 26.3,7.8 and 2.0 nmol/L,respectively. In the untreated control cells,IKK was basically phosphorylated. And phosphorylation level was transiently up - regulated after exposure to bufalin. Bay 11 - 7082, a NF- κB pathway specific inhibitor, enhanced bufalin induced -HL- 60 cell apoptosis. Conclusion :NF- κB pathway might be involved in cell proliferation and survival,and might also affect apoptosis - induced effect of bufalin.
出处 《现代肿瘤医学》 CAS 2009年第11期2039-2042,共4页 Journal of Modern Oncology
基金 国家自然科学基金(编号:30700807) 辽宁省科学技术厅基金资助项目(编号:2004225004-11)
关键词 NF—κB 蟾蜍灵 凋亡 NF - κB bufalin apoptosis
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