摘要
目的 观察三氧化二砷 (AS2 O3 )对喉癌Hep - 2细胞株诱导细胞凋亡的作用和对细胞周期的影响。方法 体外培养的Hep - 2细胞与不同浓度的As2 O3 作用 2 4、48、72h ,通过MTT还原法检测细胞的生长抑制率 ,用倒置相差显微镜、流式细胞仪、荧光显微镜研究细胞凋亡的形态学改变 ,检测细胞凋亡率并进行细胞周期分析。结果 As2 O3 可有效抑制Hep - 2细胞的生长 ,呈时间和浓度依赖性特点。形态学观察发现 ,As2 O3 诱导Hep - 2细胞凋亡。 2 μmol/LAs2 O3 作用 2 4h ,S期细胞比例增高 ,72h后 ,S期细胞明显下降 ,细胞大量凋亡。As2 O3 在低浓度时 ,阻滞细胞通过S期 ,高浓度时诱导S期细胞凋亡。结论As2 O3 可诱导Hep - 2细胞的凋亡 。
Objective To observe the apoptosis and the cell cycle in laryngeal carcinoma Hep-2 cell exposed to arsenic trioxide(As 2O 3). Methods The cell viability was measured by MTT reduction assay. The apoptic cells were observed and distinguished by light and fluorescence microscopies. Flow cytometry was used to measure the apoptic cells and the cell cycle. Results As 2O 3 affected Hep-2 cell growth apparently. The cell viability decreased dose- and time-dependently. Morphological observation indicated that As 2O 3 induced apoptosis of Hep-2 cells. The most prominent effect of As 2O 3 on cell cycle kinetics was a slowdown in S-phase transit during which cells underwent apoptosis. S-phase cell percentage increased after exposed to 2 μmol/L As 2O 3 for 24 h. With time elapsing, S-phase cell reduced. Lower concentration of As 2O 3 caused S-phase block, while higher concentration induced apoptosis of S-phase cells. Conclusion As 2O 3 can induce apoptosis of Hep-2 cells, which could be related to the cell cycle arrest.
出处
《山西医科大学学报》
CAS
2002年第3期218-220,共3页
Journal of Shanxi Medical University
