摘要
目的 研究化疗药物诱导HL60 n白血病细胞核因子 κB (NF κB)活化与凋亡的关系 ,并探讨地塞米松 (DXM )对其的影响。方法 采用电泳迁移率变动分析 (EMSA)检测细胞NF κB活化水平 ;采用TdT介导的dUTP缺口末端标记技术 (Tunel)检测细胞凋亡。结果 化疗药物诱导HL60 n白血病细胞NF κB活化与化疗药物诱导细胞凋亡明显相关 ,1μmol/LDXM能显著抑制高三尖杉酯碱 (HHT) 0 .5 μmol/L或足叶乙甙(VP 16) 1μmol/L诱导的HL60 n细胞NF κB活化 ,抑制率分别为 49.69%和 44 .3 5 % ,并增强它们诱导HL60 n细胞凋亡的作用 ,凋亡增加率分别为 5 7.5 %和 3 7.2 %。HL60 n细胞在接触化疗药物前 ,NF κB亦有一定程度的活化。结论 化疗药物在诱导HL60 n白血病细胞凋亡的同时活化NF κB ,DXM可通过抑制NF
Objective To analyze the relationship between activation of nuclear factor κB(NF κB) and apoptosis of leukemic cells induced by chemotherapeutic drugs and to explore the influence of dexamethasone (DXM). Methods Electrophoretic mobility shift assay (EMSA) was used to detect the activation of NF κB, TUNEL was adopted to observe apoptosis induced by homoharringtonine (HH) and etopside (VP 16) in HL60 n leukemic cells. Results The activation of NF κB induced by HH and VP 16 was obviously correlated to apoptosis induced by chemotherapeutic drugs in HL60 n cells. DXM(1 μmol/L) could inhibit activation of NF κB(suppressed by 57.5% and 37.2%, respectively), and increase significantly the apoptosis (increased by 49.69% and 44.35%, respectively), induced by HH(0.5 μmol/L)or VP 16 (1 μmol/L). Before exposed to chemotherapeutic agents, the activity of NF κB could be found in HL60 n cells. Conclusion Chemotherapeutic drugs induce apoptosis, and activation of NF κB of HL60 n cells. DXM enhances apoptosis on leukemic cells induced by chemotherapeutic drugs, which may be related to suppression of the activation of NF κB.
出处
《上海医学》
CAS
CSCD
北大核心
2003年第6期282-284,共3页
Shanghai Medical Journal
基金
国家自然科学基金资助项目( 39770 330 )
关键词
白血病
地塞米松
核因子—κB
化疗药物
细胞凋亡
Homoharringtonine
Etopside
Leukemic cell, HL60 n
Neuclear factor κB
Apoptosis
