二硫化二砷诱导T淋巴细胞白血病细胞株凋亡的机制研究

The mechanism of arsenic sulfide induced apoptosis of T lymphocyte leukemia cells

目的探讨二硫化二砷诱导T淋巴细胞白血病细胞株凋亡的分子机制。方法将不同浓度的二硫化二砷与T淋巴细胞白血病细胞株共培养。采用CCK-8方法测定细胞活性;AnnexinⅤ-PI方法测定细胞凋亡率,采用实时定量PCR在基因水平测定凋亡相关因子Bcl-2和Bax的表达。结果随着二硫化二砷药物浓度的增高,细胞活性减低,随着药物作用时间的延长,细胞活性逐渐减弱。其差异均有统计学意义。细胞凋亡结果显示:二硫化二砷药物浓度越高,细胞凋亡率越高,随着药物作用时间的延长,细胞凋亡率也越高。其差异均有统计学意义。实时荧光定量结果显示:与对照组比较,10μmol/L二硫化二砷与CEM细胞共孵育48 h,Bax/Bcl-2的比例升高(P<0.05)。结论二硫化二砷以时间和剂量依赖的方式抑制CEM细胞生长和诱导凋亡,诱导凋亡的机制与Bax/Bcl-2的比率增加有关。

Objective To investigate the mechanism of arsenic sulfide induced apoptosis of T lymphocyte leukemia cell line CEM. Methods CEM cells were treated with various cor^centrations of Arsenic sulfide for different time periods. Cell viability was detected by the CCK-8 assay, cell apoptosis was examined by flow cytometry. The mRNA level of Bax and Bcl-2 was detected by RT-PCR. Results We found that the T lymphocyte leukemia cells viability was significantly decreased following treatment with Arsenic sulfide for 24 h, 48 h. Along with increasing arsenic sulfide concentration, the cells viability was notably reduced when compared with the control group, and the results were statistically significant. The apoptotic rates of cells were significantly increased at 24 h and 48 h with increasing arsenic sulfide concentration, and were statistically significant. The quantitative real-time PCR results showed that the expression levels of Bax/Bcl-2 ratio were up-regulated in Arsenic sulfide-treated cells. Conclusions Arsenic sulfide inhibited proliferation and induced apoptosis of T lymphocyte leukemia cells in a dose- and time-dependent manner. The mechanism of arsenic sulfide induced apoptosis of T lymphocyte leukemia ceils was related to Bax/Bcl-2 upregulation.