论文部分内容阅读
目的：探讨紫杉醇增敏放射对胶质母细胞瘤细胞凋亡和增殖活性的影响。方法：采用人胶质母细胞瘤细胞系ＢＴ３２５。①细胞经紫杉醇和（或）照射处理后，每６ｈ收集一批细胞，至４８ｈ结束。行流式细胞术细胞凋亡分析。②细胞经紫杉醇和（或）照射处理后，培养４ｄ，作嗜银染色、ＡｇＮＯＲ计数。结果：照射后２４ｈ出现凋亡率高峰；紫杉醇加照射组的凋亡率高于单纯照射组，尤其是较低剂量照射（２和４Ｇｙ）时，相差更为显著。对照组、紫杉醇组、照射组和紫杉醇加照射组平均每个细胞的ＡｇＮＯＲ数分别为２２．８、１６．２、１５．５和６．４。结论：紫杉醇能促进放射诱导的胶质母细胞瘤细胞凋亡。紫杉醇增敏放射后残存肿瘤细胞的增殖活性显著下降。
Objective: To investigate the effect of paclitaxel-sensitized radiation on the apoptosis and proliferation of glioblastoma cells. Methods: Human glioblastoma cell line BT325 was used. ① cells after paclitaxel and (or) irradiation treatment, a collection of cells every 6h, to 48h end. Flow Cytometry Analysis of Apoptosis. ② cells treated with paclitaxel and (or) irradiation, cultured 4d for silver staining, AgNOR count. Results: The apoptotic rate peaked at 24h after irradiation. The apoptosis rate of paclitaxel plus irradiated group was higher than that of pure irradiated group, especially at the lower doses (2 and 4 Gy), the difference was more significant. The average number of AgNORs per cell in the control group, the paclitaxel group, the irradiated group and the paclitaxel plus irradiated group was 22.8, 16.2, 15.5 and 6.4, respectively. Conclusion: Paclitaxel can promote radiation-induced apoptosis of glioblastoma cells. The proliferative activity of residual tumor cells after paclitaxel sensitized radiation decreased significantly.