紫杉醇对人腺样囊性癌细胞ACC-2体外辐射增敏作用机制初探

目的 通过体外实验初步阐述紫杉醇对人腺样囊性癌细胞ACC-2的辐射增敏作用机制。方法 用克隆形成法检测不同时间-浓度条件紫杉醇和／或放射作用后的人腺样囊性癌细胞ACC-2细胞存活分数，计算辐射增敏率(SER)。用流式细胞仪分析不同时间-浓度条件下紫杉醇对细胞周期和细胞凋亡的影响。结果 10100，1000nmol紫杉醇作用24h后SER分别为1．29，1．66和1．23。紫杉醇作用时问和浓度越高，ACC-2细胞G2／M期的比率也越高。100，1000nmol紫杉醇作用24h后，G2／M期比率明显升高。10nmol紫杉醇作用24h细胞凋亡百分率20．7％。结论 紫杉醇的辐射增敏作用可能是一个多因素事件，紫杉醇的G2／M期阻滞作用和诱导细胞凋亡作用在其中起重要作用。

Mechanism of Radiosensitization of Paclitaxel on Human Adenoid Cystic Carcinoma ACC-2 Line Cells in vitro

Objective To investigate the radiosensitizing effect of paclitaxel on human adenoid cystic carcinoma ACC-2 line cell and its mechanism. Methods Human adenoid cystic carcinoma ACC-2 line cells was treated by paclitaxel and radiation at different time and dosage. The survival fraction was observed and calculated by cell colony formation, then sensitizer enhancement ratios(SER) were calculated. Paclitaxel-induced arrest of cell mitosis and apoptosis was detected with flow cytometer. Results Pretreated with 10, 100, 1000 nmol paclitaxel for 24 h, the SER were 1.29, 1.66, 1.23 respectively. The percentage of the cell population in G-2/M increased at longer paclitaxel exposure time and at higher paclitaxel concentration. But the greater ratiosensitizing effect was in 100 nmol paclitaxel(SER=1.66) than the 10 nmol or 1000 nmol groups(P<0.01). The percentage of the cell apoptosis was 20.7%, with 10 nmol paclitaxel for 24 h. Conclusion The radiosensitizing effect of paclitaxel may be a multi-mechanism event. G-2/M arrest and apoptosis play an important role in medication of paclitaxel.