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目的 :通过体外实验评价紫杉醇对人喉癌细胞系Hep 2的抑制作用。方法 :应用人喉癌细胞系Hep 2 ,将细胞暴露于不同浓度紫杉醇下 ,分别于 6、12、2 4、4 8、72h收集标本 ,进行细胞形态观察 ;流式细胞仪细胞周期分析 ;MTT法检测细胞生长情况 ,绘制细胞生长曲线 ;应用琼脂糖凝胶电泳进行检测和观察。结果 :人喉癌细胞系Hep 2在紫杉醇的作用下 ,细胞分裂阻滞在分裂期的中期 ,并诱导细胞发生凋亡 ;凋亡细胞表现为细胞固缩 ,核染色质凝聚或者断裂 ;细胞DNA裂解片段呈现典型的“阶梯状”排列的条带 ;紫杉醇对Hep 2的细胞毒性与剂量和时间有依赖关系。结论 :紫杉醇诱发人喉癌细胞凋亡与细胞分裂期阻滞密切相关 ,随浓度和时间延长 ,G2 /M期细胞的比率也增高
OBJECTIVE: To evaluate the inhibitory effect of paclitaxel on human laryngeal carcinoma cell line Hep 2 in vitro. Methods: Human laryngeal carcinoma cell line Hep 2 was used to expose the cells to different concentrations of paclitaxel. The specimens were collected at 6, 12, 24, 48 and 72 hours respectively for cell morphological observation, flow cytometry cell cycle analysis, MTT The cell growth was measured and the cell growth curve was drawn. The detection and observation were performed by agarose gel electrophoresis. Results: Hepatocarcinoma cell line Hep 2 blocked paclitaxel-induced cell division and induced apoptosis in paclitaxel-treated cells. Apoptotic cells showed cell shrinkage, condensed or broken nuclear chromatin, Lysates showed a typical “ladder-like” arrangement of bands; paclitaxel on Hep 2 cytotoxicity and dosage and time-dependent. Conclusions: Paclitaxel-induced apoptosis in human laryngeal carcinoma cells is closely related to the cell division arrest. With the increase of concentration and time, the ratio of G2 / M phase cells also increased