【摘要】 目的 探讨亚砷酸钠诱导NB4细胞凋亡的作用机制。方法 采用流式细胞术、DNA电泳和免疫印迹法研究亚砷酸钠对NB4细胞的作用。结果 ①亚砷酸钠作用的NB4细胞先阻滞在G₂ +M期，而后发生凋亡；②dUTP-FITC特异性地标记G₂ +M期NB4细胞，而且发生在G₂ +M期阻滞后；③亚砷酸钠处理NB4细胞，周期蛋白A、E、D₁ 、D₂ 和D₃ 无明显变化，周期蛋白B₁ 表达随作用时间的增加而增加；④流式细胞仪分析显示在亚砷酸钠处理的早期(16h)，有部分S期细胞表达周期蛋白B₁ ，晚期大部分高表达周期蛋白B₁ 的细胞处于G₂ +M期，有少量亚二倍体细胞高表达周期蛋白B₁ 。结论 结果提示亚砷酸钠选择性诱导G₂ +M期NB4细胞凋亡时，伴周期蛋白B₁ 表达的升高。

MA Dongchu, SUN Yinghui,MA Xiaofeng, et al. General Hospital ofShenyang Military Area, Shenyang 110015

【Abstract】 Objective To explore the mechanism ofsodium arsenite inducing apoptosis of NB4 cells. Methods The apoptosis of NB4 cells wasstudied by flow cytometry, DNA gel electrophoresis and Western blot analysis. Results ①Sodiumarsenite induced apoptosis of NB4 cells while the cells were arrested in G₂ +Mphase; ②dUTP-FITC specifically labeled NB4 cells in G₂ +M phase after thecells were treated with sodium arsenite; ③After the treatment the expressions of cyclinA, E,D₁ ,D₂ and D₃ of the NB4 cells did not changesignificantly, while the expression of cyclin B₁ was up-regulated withprolongation of the treatment; ④Some of S phase NB4 cells expressed high level cyclin B₁ during the early period of treatment (16h), but most of NB4 cells expressing high level ofcyclin B₁ were in G₂ +M phase. Conclusion Sodium arseniteselectively induced apoptosis of G₂ +M phase NB4 cells, accompanied byupregulation of cyclin B₁ .

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