三氧化二砷诱导K562细胞凋亡及其对Bcl-2和突变型P53蛋白表达的影响

Induction of Apoptosis by Arsenic Trioxide in K562 Cells and its Effect on Bcl-2 and Mutant P53 Proteins

目的：探讨Bcl-2和突变型P53蛋白在三氧化二砷（As2O3）诱导K562细胞凋亡中的作用及机制。方法：分别以1、2、4、8、16μmol/L的As2O3诱导K562细胞凋亡,MTT法检测24、48、72h时细胞增殖抑制率,DNAl-adder法检测细胞凋亡,AnnexinV/PI染色结合流式细胞术检测细胞凋亡率,流式细胞术检测Bcl-2和突变型P53表达。结果：不同浓度的As2O3对K562细胞具有增殖抑制作用,且呈现时间剂量依赖性。DNA ladder及AnnexinV/PI法结果显示4~16μmol/L的As2O3作用24h均可诱导K562细胞凋亡,且呈剂量依赖性。As2O3诱导K562细胞凋亡同时伴随着胞浆Bcl-2和突变型P53表达降低。结论：As2O3可诱导K562细胞凋亡,Bcl-2和突变型P53表达降低可能与其有关。

Objective ： To investigate the apoptosis inducing activity of arsenic trioxide and its effect on the expression of Bcl - 2 and mutant P53 proteins. Methods ： K562 cells were treated with arsenic trioxide at 1,2,4,8,16umol/L. Cell growth inhibitory rate was detected by MTT colorimetric assay every 24 hours. Apoptosis rate was analyzed by DNA ladder and Annexin V/PI fluorescence staining together with flow cytometry. Changes in expression of Bcl -2 and mutant P53 protein was assayed by flow cytometry. Results： MTT tests showed K562 cell proliferation was significantly inhibited by arsenic trioxide in time and dose - dependent fashion. Marked apoptosis was detected by DNA ladder and Annexin V/PI in K562 cells after treatment by arsenic trioxide at 4,8,16umol/L after 24 hours and increased in a dose-dependent manner. The expression of Bcl - 2 and mutant P53 protein decreased in K562 cells induced by arsenic trioxide for 24 hours. Conclusion：Bcl -2 and mutant P53 protein probably correlated with the activation of apoptosis in K562 cells induced by arsenic trioxide.