Tamoxifen联合γ线照射对脑胶质瘤细胞的增殖抑制及凋亡诱导作用  

Effect of tamoxifen combined with ^(60)Co γ-irradiation on proliferation inhibition and apoptosis induction in human glioma SHG-44 cells

作　　者：宁萍[1,2] 刘芬菊[1,2] 薛景1 

机构地区：[1]苏州大学放射医学与公共卫生学院 [2]江苏省放射医学与防护重点实验室江苏苏州215123

出　　处：《辐射研究与辐射工艺学报》2006年第3期183-187,共5页Journal of Radiation Research and Radiation Processing

基　　金：苏州大学医学发展基金重点项目(EE126031);江苏省放射医学重中之重学科(FY2004)资助

摘　　要：研究三苯氧胺(Tamoxifen,TAM)对人脑胶质瘤细胞辐射增敏作用及诱导细胞凋亡。用3H-TdR掺入法、免疫组织化学法、流式细胞术和激光共聚焦显微镜扫描技术检测细胞DNA合成、雌激素受体表达、细胞凋亡及凋亡的形态学特征。结果表明,TAM能抑制细胞DNA合成,与60Coγ线联用抑制作用增强,表现出协同作用。TAM能诱导细胞凋亡,其凋亡率随TAM浓度的升高而增高,凋亡细胞核固缩和核碎裂,可见凋亡小体。而免疫组化结果显示SHG-44细胞不表达雌激素受体。以上结果表明TAM可能通过诱导细胞凋亡途径来增加细胞的辐射敏感性,而与雌激素受体途径无关。To study radiosensitizing effect and apoptosis induction of tamoxifen on human glioma cells, ^3H-TdR incorporation assay, flow cytometry, laser confocal microscope and Immunohistochemistry were used to investigate the inhibition effect on DNA synthesis, apoptosis and estrogen receptor expression. Experiment results suggested that tamoxifen could inhibit DNA synthesis in SHG-44 cells,the combination of tamoxifen and ^60Co γ-irradiation showed a synergistic action on it. Tamoxifen could also induce the apoptosis, and the apoptosis rate increased along with tamoxifen concentration was elevated, so morphologyical changes, such as karyopyknosis, nuclear fragmentation and apoptotic body were observed. However, SHG-44 cells did not express estrogen receptor. The above results revealed that tamoxifen can sensitize SHG-44 cells to gama radiation, which might be related with apoptosis pathway instead of the estrogen receptor-mediated process.

关 键 词：三苯氧胺 脑胶质瘤细胞 辐射增敏 凋亡 

分 类 号：R811.5[医药卫生—放射医学] R730.5[医药卫生—临床医学]