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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；②ｄＵＴＰＦＩＴＣ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。
Aim To investigate the mechanism of sodium arsenite-induced NB4 cell apoptosis. Methods The effects of sodium arsenite on NB4 cells were studied by flow cytometry, DNA electrophoresis and Western blotting. Results ① The arsenite-induced NB4 cells were arrested in G2 + M phase and then apoptosis occurred. ②UTPFITC specific labeling of G2 + M NB4 cells, and G2 + M phase arrest; ③ sodium arsenite treatment of NB4 Cytokines A, E, D1, D2 and D3 showed no significant change, and the expression of cyclin B1 increased with the increase of time. (4) Flow cytometry analysis showed that in the early stage of arsenite treatment (16h) S phase cells express cyclin B1, most of late phase cyclin B1 cells are in G2 + M phase, and a small amount of subdiploid cells express cyclins B1. Conclusion The results suggest that sodium arsenite selectively induces the increase of cyclin B1 expression in G2 + M NB4 cells.