三氧化二砷诱导HL-60细胞凋亡效应及抑制细胞ERK的活性

目的:初步探讨三氧化二砷(arsenic trioxide,As2O3)促进HL-60细胞凋亡及其可能机制.方法:不同浓度的As2O3(0、2.5、5、10 μmol/L)作用于HL-60细胞24h后,MTT法检测细胞增殖,流式细胞术检测细胞凋亡,Western blot检测Caspase-3活化、ERK活性和cyclinD1蛋白的表达,RT-PCR法检测cyclinD1 mRNA的表达.结果:As2O3可抑制HL-60细胞增殖,诱导HL-60细胞的凋亡,并呈浓度依赖性 (P<0.05);As2O3可使HL-60细胞Caspase-3激活,并抑制ERK活性,但不能下调cyclinD1的表达(P>0.05).结论:As2O3能抑制HL-60细胞增殖,并诱导其凋亡,其效应可能与As2O3抑制HL-60细胞ERK活性有关.

Arsenic trioxide induces apoptosis and inhibit activity of ERK in HL-60 cells

Objective:To explore the effect of arsenic trioxide on induction of HL-60 cell apoptosis and its possible mechanism.Methods: HL-60 cells were treated with different concentration of arsenic trioxide for 24 hours(0,2.5,5,10 μmol/L),the proliferative activity of HL-60 cells was tested by MTT,the apoptosis of HL-60 cells was assayed by flow cytometry with Annexin V-FITC/PI double labeling,the actived Caspase-3 and the expression of phospho-ERK and cyclinD1 at protein level in HL-60 cells were detected by Western blot,the level of cyclinD1 mRNA in HL-60 cells was determined by RT-PCR.Results: Arsenic trioxide could inhibit the proliferation of HL-60 cells and induce the apoptosis of HL-60 cells in concentration-dependent manners(P<0.05),arsenic trioxide could activate Caspase3 and suppress the activity of ERK,but did not down-regulate the expression of cyclinD1(P>0.05).Conclusion: Arsenic trioxide inhibits the proliferation and induces the apoptosis of HL-60 cells,its mechanism may be related with suppressing activation of ERK.