沙利度胺增强X射线对胶质瘤U251细胞辐射敏感性机制的研究  

The study on the mechanism of enhanced radio-sensitivity of glioma cell U251 by thalidomide

作　　者：于静萍[1,2] 孙美玲[1] 孙苏平[2] 尹小祥[1] 刘海燕[1] 张昊文[1] 冯爽[1] 刘芬菊[1] 

机构地区：[1]苏州大学医学部放射医学与公共卫生学院,苏州215123 [2]常州市第二人民医院,常州213003

出　　处：《辐射研究与辐射工艺学报》2010年第6期368-372,共5页Journal of Radiation Research and Radiation Processing

基　　金：国家自然科学基金(30870585);常州市青年科技培养计划(CQ2008006);常州市社会发展指导性项目(CS2008920)资助

摘　　要：为探讨沙利度胺增强X射线对胶质瘤U251细胞DNA合成抑制及增强辐射敏感性的作用机制,采用甲基噻唑基四氮唑盐(Methyl thiazolyl tetrazolium,MTT)法检测沙利度胺对胶质瘤U251细胞存活率的影响;H3-胸腺嘧啶(H3-Thymidine,H3-TdR)掺入法研究沙利度胺单用及联合X射线对U251细胞DNA合成抑制作用;逆转录聚合酶链反应(Reverse transcriptase PCR,RT-PCR)检测与肿瘤发生密切相关的血管内皮生长因子(Vascular endothelia growth factor,VEGF)mRNA的相对表达水平;Western blot分析VEGF蛋白表达变化。结果表明,沙利度胺对胶质瘤细胞的增殖抑制作用随着浓度的增高和时间的延长而缓慢增加。沙利度胺抑制U251细胞DNA合成,联合X射线照射后,具有协同作用;沙利度胺可以抑制VEGFmRNA的表达,随着沙利度胺浓度的增加,表达量减少,联合X线照射,减少更明显;低剂量辐射在24 h内可以诱导VEGF蛋白的表达,随着时间的延长表达减少。实验证明沙利度胺对脑胶质瘤U251细胞属低细胞毒性药物,能够抑制肿瘤细胞DNA合成。In order to investigate the inhibition of DNA synthesis and the mechanism of thalidomide enhanced radio-sensitivity on glioma U251 cells,survival rate of the cells was assessed by MTT assay;and 3H-TdR incorporation assay was used to investigate the inhibition of DNA synthesis by thalidomide alone and combined with X-rays;VEGF mRNA expressions were evaluated using RT-PCR assay.Protein expression（VEGF） was detected by Western blot analysis.Thalidomide inhibited DNA synthesis depending on the concentration of thalidomide and radiation dose.Thalidomide markedly down-regulated VEGF mRNA combined with X-rays in which a synergistic action appeared.Low dose X-rays can induce VEGF protein expression in 24 h.Thalidomide was a low toxicity to U251 cells.Thalidomide inhibited DNA synthesis of U251 cells.

关 键 词：沙利度胺 胶质瘤U251细胞 DNA合成 血管内皮生长因子 

分 类 号：R73-3[医药卫生—肿瘤] R739.4[医药卫生—临床医学]