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目的 研究不同浓度的亚砷酸对NB4 细胞凋亡的影响。方法 采用流式细胞术、DNA电泳和免疫印迹研究测定亚砷酸对NB4 细胞凋亡作用。结果 (1)经 0 8～ 8μmol·L-1亚砷酸作用 16h后 ,NB4 细胞生存力为 95 0 %以上 ,有“梯状”DNA电泳带和亚二倍体峰 ,细胞在G2 期阻滞 ,但bcl 2表达明显下调 ;(2 )浓度在 10～ 80 μmol·L-1时 ,虽然凋亡广泛发生 ,bcl 2表达明显下调 ,但细胞生存率也降至 31 2 % ;(3)浓度在 40 0 μmol·L-1时 ,细胞生存力为 (80 3± 8 9) % ,无“梯状”电泳带、细胞周期阻滞和bcl 2下调 ,76 6 %细胞被dUTP FITC标记 ,但荧光强度低 ,这也说明在高浓度时 ,亚砷酸诱导凋亡的作用受到了抑制。结论 提示亚砷酸不仅可以诱导NB4 细胞凋亡也可以抑制其凋亡。在低浓度时 ,亚砷酸诱导凋亡的作用强于其抑制凋亡。高浓度时相反。因此 ,通过有机化或化学结构的改变降低其抑制作用可能有助于提高疗效。
Objective To study the effect of different concentrations of arsenic trioxide on the apoptosis of NB4 cells. Methods Apoptosis of NB4 cells induced by arsenious acid was determined by flow cytometry, DNA electrophoresis and Western blotting. Results (1) The NB4 cells had a viability of more than 95% after being exposed to arsenous acid of 0.8 to 8 μmol·L-1 for 16 h. There were “ladder” DNA bands and subdiploid peaks. The cells were arrested at the G2 phase. Hysteresis, but bcl 2 expression was significantly down-regulated; (2) At a concentration of 10 to 80 μmol·L-1, although apoptosis occurred extensively, bcl 2 expression was significantly downregulated, but the cell survival rate also decreased to 31 2%; (3) At a concentration of 40 μmol·L-1, the cell viability was (80 3 ± 8 9)%. There was no “step-like” electrophoresis band, cell cycle arrest, and bcl 2 downregulation. 76.6% of cells were labeled with dUTP FITC. However, the low fluorescence intensity indicates that the effect of arsenic trioxide on apoptosis is inhibited at high concentrations. Conclusion It is suggested that arsenic trioxide can not only induce apoptosis but also inhibit apoptosis in NB4 cells. At low concentrations, arsenic trioxide induced apoptosis more strongly than it inhibited apoptosis. The opposite is true at high concentrations. Therefore, reducing its inhibitory effect through organic or chemical structure changes may help improve the efficacy.