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目的 :探讨砷制剂诱导NB4 细胞凋亡的途径及调控因子。方法 :将NB4 细胞与不同浓度的As2 O3 共同孵育 ,在不同时间 ,用比色法检测NB4 细胞胞浆内Caspase 3、 6、 8的活性 ,并用流式细胞仪检测细胞内转录因子NF κB的表达 ,同时作细胞周期分析及DNA梯度鉴定As2 O3 的致凋亡作用。结果 :NB4 细胞在 1.0、2 .0 μmol/LAs2 O3 的诱导下 ,于 16～ 2 4h的时段内均有明显的凋亡现象 ;期间 ,Caspase 3, 6 , 8被活化 ,较对照组差异有显著性意义 (P <0 .0 5 ) ;不同的时间点Caspase家族成员激活顺序不同 ,这种时间上的差异有显著性意义 (P <0 .0 5 ) ;NF κB在 6～ 16h期间的对照组和加药组 (1.0 μmol/LAs2 O3 )均有表达 ,加药组较对照组明显减低 (P <0 .0 5 ) ,但无时间依从性。结论 :As2 O3 可抑制NF κB的表达 ,诱发凋亡 ;NB4 细胞通过Caspase途径凋亡 ,顺序可能为Caspase 8→Caspase 6→Caspase 3,其中 ,Caspase 6是活性较高的成员之一 ;As2 O3 作为NF κB的有效抑制剂 ,可能对多种肿瘤有潜在的治疗意义。
Aims: To explore the pathways and regulators of apoptosis induced by arsenic in NB4 cells. Methods: NB4 cells were incubated with different concentrations of As2 O3. The activity of Caspase 3, 6 and 8 in the cytoplasm of NB4 cells was detected by colorimetric assay at different time points. The expression of NFκB Expression, at the same time for cell cycle analysis and DNA gradient identification of apoptosis induced by As2 O3. Results: Under the induction of 1.0,2. 0 μmol / L As 2 O 3, NB4 cells showed obvious apoptosis in 16 ~ 24 hours. Caspase 3, 6 and 8 were activated in NB4 cells compared with the control group (P <0.05). There was a significant difference in the activation order of Caspase family members at different time points (P <0.05), while there was no significant difference in the expression of NF-κB between 6 ~ 16h The control group and the dosing group (1.0 μmol / L As 2 O 3) were all expressed, and the dosing group was significantly lower than the control group (P <0.05), but no time-dependent. CONCLUSION: As2 O3 can inhibit the expression of NF-κB and induce apoptosis. The apoptosis of NB4 cells via Caspase pathway may be Caspase 8 → Caspase 6 → Caspase 3, among which Caspase 6 is one of the more active members. As 2 O 3 As a potent inhibitor of NF-κB, it may have potential therapeutic implications for a variety of tumors.