摘要
目的 :研究地塞米松 (DXM)和长春新碱 (VCR)对阿糖胞苷 (Ara C)诱导HL60 n白血病细胞凋亡与核因子 κB(NF κB)活化的影响。方法 :采用TdT介导的dUTP缺口末端标记 (Tunel)和DNA电泳技术检测HL60 n细胞凋亡 ;采用电泳迁移率变动分析 (EMSA)检测HL60 n细胞NF κB活化水平。结果 :Ara C同时具有诱导HL60 n细胞凋亡和NF κB活化的作用 ;DXM 1 μmol/L和VCR 0 .1 μmol/L能显著增强Ara C诱导的HL60 n细胞凋亡和抑制Ara C诱导的HL60 n细胞的NF κB活化 ,细胞凋亡增强率分别为 39.1 %和 59.2 % (均P <0 .0 5) ,NF κB活化抑制率分别为 31 .0 %和 47.0 % (均P <0 .0 5)。结论 :Ara C诱导HL60 n细胞凋亡的同时激活NF κB ;DXM和VCR可通过抑制NF κB活化 ,增强其诱导HL60
Purpose:To explore effects of dexamethasone and vincristine on apoptosis and activation of NF κB of HL60 n cells induced by cytosine arabinoside (Ara C). Methods:Apoptosis induced by Ara C in HL60 n cells was analysed by Tunel and DNA electrophoresis. The DNA binding activation of NF κB of HL60 n cells was determined by electrophoretic mobility shift assay(EMSA).Results:The apoptosis and activation of NF κB of HL60 n cells could be induced by Ara C. Dexamethasone 1μmol/L and vincristine 0.1μmol/L increased significantly the apoptosis induced by Ara C (increased by 39.1% and 59.2%, P <0.05, respectively), Meanwhile, dexamethasone and vincristine suppressed activation of NF κB of HL60 n cells induced by Ara C (suppressed by 31.0 % and 47.0%, P <0.05, respectively).Conclusions:Ara C induced apoptosis, and at the same time, induced activation of NF κB of HL60 n cells. The mechanism of Dexamethasone and vincristin in increased apoptosis of leukemic cells may be related to suppressing activation of NF κB of HL60 n cells.
出处
《中国癌症杂志》
CAS
CSCD
2003年第2期106-108,111,共4页
China Oncology
基金
国家自然科学基金( 39770 330 )资助
