硼中子俘获疗法诱导SHG44胶质瘤细胞凋亡  

Boron neutron capture therapy induced apoptosis in SHG44 glioma cells

作　　者：王鹏[1] 章翔[1] 江新标[2] 程光[1] 赵英[2] 甄海宁[1] 王剑博[1] 曹锐峰[1] 

机构地区：[1]第四军医大学西京医院全军神经外科研究所,西安710032 [2]西北核技术研究所

出　　处：《中华放射医学与防护杂志》2008年第5期484-487,共4页Chinese Journal of Radiological Medicine and Protection

基　　金：国家自然科学基金资助项目（10375047）

摘　　要：目的探讨硼中子俘获疗法（BNCT）是否抑制人脑胶质瘤细胞SHCCM增殖及其作用机制。方法BNCT作用后，应用四甲基偶氮唑蓝比色法检测SHG44细胞的增殖抑制，采用光镜、电镜、荧光显微镜观察细胞的形态学变化。应用流式细胞仪检测SHG44细胞的凋亡率，以Westernblot检测细胞表达Bcl-2、B“蛋白的变化。结果BNCT对SHG44细胞的增殖抑制作用呈剂量依赖性。BNCT4和8Gv后48h流式细胞仪检测凋亡率分别为63．2％和88．3％。BNCT作用后，Bax蛋白表达增高，Bcl-2蛋白表达下降。结论BNCT对胶质瘤细胞SHG44具有明显的增殖抑制及诱导凋亡作用，并使Bax蛋白表达上调、Bcl-2蛋白表达下凋。Objective To investigate the inhibition of boron neutron capture therapy（BNCT） on SHG44 glioma cell line and its mechanism. Methods Methyl thiazolyl tetrazolium （MTF） assay was used to measure the level of the proliferation of SHG44. HE staining, Hoechst33342 fluorescence staining, transmission electron microscope（TEM） were applied to observe the changes in cell morphology. The effects of BNCT on cell apoptotic rate was observed by flow cytometer （FCM）. The expression of Bcl-2 and Bax protein was measured by Western blot. Results The proliferation of SHG44 was obviously inhibited by BNCT in a dose-dependent manner. The results of FCM showed that the apoptotic cell rate 48 h after irradiation with 4 and 8 Gy 63.2% and 88.3%, respectively. Western blot analysis showed BNCT promoted Bax protein expression, but inhibited Bcl-2 expression. Conclusions BNCT inhibits the proliferation of SHG44 cell, induces apoptosis and promote the expression of Bax but inhibits the expression of Bcl-2.

关 键 词：硼中子俘获疗法 SHG44细胞 凋亡 

分 类 号：R739.4[医药卫生—肿瘤]