环氧合酶-2抑制剂NS-398对食管癌细胞放射增敏作用及机制初探  

Radiosensitization of cyclooxygenase-2 selective inhibitor NS-398 in esophageal carcinoma cell and its mechanism

作　　者：李胜保[1] 吴清明[1] 王小虎[1] 谢国建[1] 

机构地区：[1]郧阳医学院附属太和医院消化内科,湖北十堰442000

出　　处：《中华放射肿瘤学杂志》2005年第4期350-352,共3页Chinese Journal of Radiation Oncology

摘　　要：目的探讨COX2选择性抑制剂NS398对食管癌细胞株EC9706放射敏感性的影响及作用机制。方法选用高表达COX2的人食管癌细胞株EC9706为靶细胞,加入不同浓度(10、20、50、100μmol/L)的NS398,分别作用24、48h,用直线加速器分别给予0、2、4、6、8、10Gy剂量照射,采用成克隆实验分析增敏效应,用DNA片段分析法及流式细胞术检测细胞凋亡情况。结果用10、20、50、100μmol/L的NS398作用24、48h均能检测到放射增敏作用,其放射增敏比(Dq比)分别为1.11、1.24、1.40、1.54和1.11、1.27、1.58、1.67,呈剂量和时间依赖性;同时使细胞凋亡率增加。结论NS398能增强人食管癌细胞株EC9706对放射的敏感性,其增敏机制与抑制亚致死性损伤修复和诱导细胞凋亡增加有关。Objective Objective To study the influence of NS-398,a selective cyclooxygenase-2 inhibitor on the radiosensitivity of human esophageal carcinoma cell line EC9706 cell. Methods EC9706 cell, highly expressing COX-2, had been incubated with NS-398 at 10、20、50 and 100?μmol/L for 24?h or 48?h before irradiation ranging from 0 to 10?Gy. Cell survival was measured by a standard clonogenic assay after 8 days of incubation. Apoptotic percentage was measured by FCM and DNA fragmentation by agarose electrophronesis. Results The senstization enhancement ratios (ratio of D_q) in EC9706 cell were 1.11, 1.24, 1.40, 1.54 at 10, 20, 50, 100?μmol/L of NS-398 for 24?h pre-incubation and 1.11, 1.27, 1.58, 1.67 for 48?h pre-incubation, which showed a dose-dependant and time-dependant manner. FCM analysis revealed a higher sub-G_1 cell peak in NS-398 group after irradiation. Agarose electrophronesis showed a marked ladder. Radiation-induced apoptosis was enhanced by NS-398 (P<0.05 or P<0.001). Conclusions NS-398, a COX-2 inhibitor, can enhance the radiosensitivity of esophageal carcinoma cell. The mechanism may be associated with induced apoptosis of EC9706 cells.

关 键 词：环氧合酶-2 抑制剂 NS-398 食管癌 肿瘤细胞 放射增敏作用 消化系统 

分 类 号：R735.1[医药卫生—肿瘤]