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目的 研究四硫化四砷对NB4细胞的促凋亡作用及这一过程中早幼粒细胞白血病 维甲酸受体α(PML RARα)融合基因及其表达产物的变化。方法通过细胞形态学观察 ,流式细胞仪检测及DNA电泳等方法观察四硫化四砷对NB4细胞的诱导凋亡作用 ,用荧光染色体原位杂交技术 ,反转录PCR及Western印迹技术测定这一过程中PML RARα融合基因及其表达产物的改变。结果 四硫化四砷在 0 .5～ 3μmol·L- 1之间能诱导NB4细胞凋亡 ,在此过程中 ,PML RARα融合基因无明显变化 ,但PML RARα融合蛋白和野生型RARα蛋白的表达明显减少。结论 四硫化四砷能诱导NB4细胞凋亡 ,其作用靶点可能在PML RARα融合蛋白和野生型RARα蛋白。
Objective To study the apoptosis-promoting effect of arsenic tetrathionate on NB4 cells and the changes of PML RARα fusion gene and its expression products in this process. Methods The apoptotic effects of arsenic tetrathionate on NB4 cells were observed by morphological observation, flow cytometry and DNA electrophoresis. Fluorescent chromosomal in situ hybridization, reverse transcription PCR and Western blotting were used to detect the apoptosis of NB4 cells. PML RARα fusion gene and its expression product changes. Results Arsenic tetrathiazide could induce the apoptosis of NB4 cells in the range of 0.5 ~ 3μmol·L-1. During the process, there was no significant change in the fusion gene of PML RARα, but the expression of RARα fusion protein and wild-type RARα protein was significantly cut back. Conclusion Arsenic tetra-sulphide can induce the apoptosis of NB4 cells, and its target may be PML RARα fusion protein and wild-type RARα protein.