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目的 研究地塞米松 (DXM)和长春新碱 (VCR)对高三尖杉酯碱 (HH)诱导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缺口末端标记技术(TUNEL)、DNA电泳方法观察HH诱导K5 6 2 n细胞凋亡 ,采用电泳迁移率变动分析 (EMSA)观察HH诱导K5 6 2 n细胞NF κB活化。结果 用 (0 5、5、5 0 ) μmol/L的HH均能诱导K5 6 2 n细胞凋亡率分别为 (30 0 0± 3 34,4 7 13± 3 18,6 8 6 3± 8 14 ) % ,与对照组相比 ,有良好的浓度依赖关系 (P <0 0 5 ) ;DXM 1μmol/L和VCR 0 1μmol/L本身无诱导K5 6 2 n细胞凋亡的作用 ,但均能增强HH 0 5μmol/L诱导的K5 6 2 n细胞凋亡 ,凋亡增加率分别为 85 8%和 114 6 % (P值均 <0 0 5 )。K5 6 2 n细胞未经药物诱导NF κB也有轻度活化 ;HH 0 5 μmol/L可明显诱导K5 6 2 n细胞NF κB活化 ,DXM 1μmol/L和VCR 0 1μmol/L能显著抑制HH 0 5 μmol/L诱导的NF κB活化 ,抑制率分别为 32 0 %和39 4 % (P值均 <0 0 5 )。结论 HH诱导K5 6 2 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K5 6 2 n细胞凋亡的作用。
Objective To investigate the effects of dexamethasone (DXM) and vincristine (VCR) on homoharringtonine (HH) -induced apoptosis and the activation of NF-κB in leukemia cells. Methods The TdT-mediated dUTP nick end labeling (TUNEL) and DNA electrophoresis were used to observe the apoptosis of K562-n cells induced by HH. The activation of NF-κB in K562-n cells was observed by electrophoretic mobility shift assay (EMSA) Results The apoptotic rates of K562 2 n cells induced by (0, 5, 5, 50) μmol / L HH were (30 0 ± 3 34, 47 13 ± 3 18, 6 8 6 3 ± 8 (P <0.05). DXM 1 μmol / L and VCR 0 1 μmol / L did not induce the apoptosis of K562 2 n cells in vitro, but both of them could The apoptosis of K562n cells induced by HH 0 5μmol / L was enhanced by 85.8% and 114.6%, respectively (all P <0.05). K5 6 2 n cells also showed slight activation of NF κB. KH 6 μmol / L HH 0 5 μmol / L could obviously induce NF κB activation in K5 6 2 n cells. DXM 1 μmol / L and VCR 0 1 μmol / L could significantly inhibit HH 0 5 The activation of NF-κB induced by μmol / L was 32 0% and 39 4%, respectively (P <0.05). Conclusion HH induces apoptosis of K5 6 2 n cells and activates NF κB. DXM and VCR can enhance the apoptosis of K5 6 2 n cells by inhibiting NF κB activation.