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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 ,与细胞周期阻滞有关
Objective: To observe the effect of arsenic trioxide (As 2 O 3) on Hep-2 cell line and vincristine-induced multidrug resistance Hep-2 r cell line and its effect on cell cycle. Methods: The drug-resistant Hep-2r cells were screened by increasing concentration of vincristine (VCR). Cells cultured in vitro were incubated with different concentrations of As2 O3 for 2, 44 and 72 hours. The cell growth inhibition rates were determined by MTT assay. Morphological changes of apoptosis were observed by light microscopy, flow cytometry and fluorescence microscopy. Cell apoptosis rate was measured and cell cycle analysis was performed. Results: As2 O3 could effectively inhibit the growth of Hep-2 and Hep-2r cells in a time and concentration-dependent manner. Morphological observation showed that As2 O3 induced Hep-2 and Hep-2r cell apoptosis, Hep-2 and Hep-2r cells had no significant difference on As2 O3 sensitivity. After treated with 2 μmol / L As 2 O 3 for 24 h, the proportion of S phase cells was increased. After 72 h, the S phase cells were significantly decreased and the cells were largely apoptotic. As2 O3 in the early role of arrest cells through the S phase, with the extension of time, S phase apoptosis induced. Conclusion: As2 O3 can induce the apoptosis of Hep-2 and Hep-2r cells, which is related to the cell cycle arrest