LM-1685对人肺腺癌细胞A549的放射增敏作用  

Radiosensitizing effects of cyclooxygenase.2 selective adenocarcinoma cells

作　　者：盛李明[1] 水永杰[1] 钟献[1] 沈俐[1] 魏启春[1] 

机构地区：[1]浙江大学医学院附属第二医院肿瘤放疗科浙江大学肿瘤研究所,杭州310009

出　　处：《中华放射医学与防护杂志》2008年第4期323-326,共4页Chinese Journal of Radiological Medicine and Protection

基　　金：国家自然科学基金资助项目（30470501）

摘　　要：目的 观察环氧合酶-2（COX-2）抑制剂对肺癌细胞的放射增敏作用。方法 COX-2抑制剂LM-1685作用于体外培养的肺癌细胞A549，噻唑蓝（MTT）法检测其对肺癌细胞的抑制效果，克隆形成法检测放射敏感性，流式细胞术检测细胞周期变化。结果COX-2抑制剂LM-1685具有明显的抑制A549细胞增殖的作用，其效应呈时间和剂量依赖性，50μmol／LLM-1685在有或没有IL-1β作用下对A549细胞均有放射增敏作用，其放射增敏比分别为1．12、1．06。50μmol／LLM-1685能去除X射线导致的A549细胞G2／M期阻滞。结论 COX-2抑制剂对肺癌细胞A549具有放射增敏作用，放射增敏机制可能与去除G2／M期阻滞有关。Objective To investigate the radiosensitizing effects of cyclooxygenase-2 selective inhibitor LM-1685 on A549 cells in vitro. Methods A549 human lung adenocarcinoma cell line was used in this study. Cell growth kinetics was determined using MTT assay. Cell survival was analyzed by clonogenic assay. The change of cell cycle was measured by flow cytometry. Results LM-1685 inhibited the growth of A549 cells, showing a dose-dependent and time-dependent manner. LM-1685 （50 μmol/L）, either with or without IL-1β, showed the radiosensitizing effects on A549 cells, and the sensitizing enhancement ratio （SER） was 1.12 and 1.06, respectively. LM-1685 （50 μmol/L） abrogated radiation-induced GflM arrest of the tested A549 cells. Conclusions Cyclooxygenase-2 selective inhibitor can enhance the radiosensitivity of A549 cell line. Abrogation of radiation-induced G2/M arrest could be part of the mechanism.

关 键 词：肺癌 放射治疗 COX-2抑制剂 放射增敏 

分 类 号：R734.2[医药卫生—肿瘤] R730.55[医药卫生—临床医学]