三氧化二砷诱导喉癌Hep-2耐药细胞凋亡的研究  

Study of arsenic trioxide induced apoptosis in laryngeal carcinoma resistance Hep-2 cell

作　　者：陈勇[1] 王天铎[1] 陈明[2] 李瑞玉[2] 林本良[2] 

机构地区：[1]山东大学齐鲁医院耳鼻咽喉科,济南250012 [2]福建省立医院耳鼻咽喉科

出　　处：《山东医大基础医学院学报》2002年第3期139-141,共3页

摘　　要：目的 :观察三氧化二砷 (As2 O3 )对喉癌Hep -2细胞株和长春新碱诱导的多药耐药Hep -2r细胞的作用和对细胞周期的影响。方法 :用长春新碱(VCR)递增药物浓度法筛选耐药细胞Hep -2r,体外培养的细胞与不同浓度的As2 O3 作用 2 4、48、72h,通过MTT还原法检测细胞的生长抑制率 ,用光学显微镜、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细胞和Hep-2r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和Hep-2r细胞凋亡 ,Hep -2和Hep -2r细胞对As2 O3 的敏感性无显著差异。2 μmol/LAs2 O3 作用 2 4h时 ,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 在作用早期 ,阻滞细胞通过S期 ,随着时间的延长 ,诱导S期细胞凋亡。结论 :As2 O3 可诱导Hep -2细胞和Hep-2r细胞凋亡 。Objective:To observe the apoptosis and the cell cycle in laryngeal carcinoma Hep-2 cell and resistance Hep-2r exposed to arsenic trioxide(As 2O 3). Method:The resistance cell line Hep-2r was established by exposed to vincrestine(VCR) with increasing concentration.The Hep-2 and Hep-2r cell viability were measured by MTT reduction assay.The apoptic cells were observed and distinguished by light microscopy and fluorescence microscopy.Flow cytometry was used to measure the apoptic cells and the cell cycle.Result:As 2O 3 affected Hep-2 and Hep-2r cell growth apparently.The cell viability increased with dose and time dependence.The cell viability appeared no significant difference between Hep-2 and Hep-2r cell.Morphological observation indicated that As 2O 3 induced apoptosis of Hep-2 and Hep-2r cells.The most prominant effect of As 2O 3 on cell cycle kinetics was a slowdown in S-phase transit during which cells undergone apoptosis.S-phase cell percentage increased after exposed to 2μmol/L As 2O 3 for 24h.With time elapsing,S-phase cell reduced.Conclusion:As 2O 3 can induce apoptosis of Hep-2 and Hep-2r cells,which can be related to the cell cycle arrest.

关 键 词：喉肿瘤 砷剂 细胞凋亡 细胞周期 多药耐药 

分 类 号：R739.65[医药卫生—肿瘤]