对乙酰氨基酚对不同脑胶质瘤细胞的放射增敏作用及其机制研究  

Radiosensitization of acetaminophen on human glioma cell lines and its mechanism

作　　者：周菊英[1] 涂彧[2] 徐晓婷[1] 俞志英[1] 秦颂兵[1] 王利利[1] 李莉[1] 周乐源[1] 

机构地区：[1]苏州大学附属第一医院肿瘤放疗科,215006 [2]苏州大学放射医学与公共卫生学院

出　　处：《中华放射医学与防护杂志》2008年第5期502-505,共4页Chinese Journal of Radiological Medicine and Protection

基　　金：国家自然科学基金资助项目（30670638）

摘　　要：目的探讨对乙酰氨基酚联合放射对人恶性脑胶质瘤细胞2种细胞的放射增敏效应及其可能的机制。方法以人恶性脑胶质瘤细胞株SHG-44及其接受10Gy6MVX射线照射后的存活后代细胞SHG-4410 Gy为研究对象，采用免疫细胞化学和RT-PCR检测2株细胞COX-2的表达，集落形成实验测定对乙酰氨基酚对细胞的放射增敏作用。结果HG-4410Gy较SHG-44的放射敏感性低（P〈0．01）；免疫细胞化学染色SHG-44和SHG-4410Gy细胞的胞质及胞膜均有COX-2蛋白的表达，且后者明显高于前者；RT-PCR检测SHG-4410Gy中COX-2mRNA表达水平明显高于SHG-44细胞，与放射敏感性有显著的相关性（r=0．976，P〈0．01）；对乙酰氨基酚联合放疗分别作用于SHG-44和SHG-4410Gy细胞，与单纯照射组相比，显示了放射增敏作用，SHG-44细胞D0值和Dq值增敏比分别为1．09和1．11，SHG-4410Gy的SER分别为1．12和3．01。结论人恶性脑胶质瘤细胞株SHG-44及其照射存活后代细胞均有COX-2表达，且对辐射耐受的存活后代细胞中COX-2明显增高；对乙酰氨基酚可通过抑制COX-2的表达增加人脑胶质瘤SHG-44细胞尤其是其照射后代细胞的放射敏感性。Objective To investigate the radiosensitivity enhancement and underlying mechanism of acetaminophen , non-selective cyclooxygenase （COX）-2 inhibitor, on human glioma cell lines expressing differential COX-2 levels. Methods The SHG-44 cells were irradiated with a dose of 10 Gy using 6 MV X-rays generated by linar accelerator. The progeny of the cells were cultured and named SHG-4410 Gy - COX-2 mRNA and protein expression of SHG-44 and SHG-4410 Cy were detected by RT-PCR and immunocytochemisty staining. Clongenic assay was used for radiation survival experiment. Results The declined radiosensitivity was detected in the SHG-4410 Gy. RT-PCR showed that the expression of COX-2 mRNA in SHG-4410 Gy significantly higher than that in SHG-44 cells （ P 〈 0.01 ）. The cell inhibition induced by Acetaminophen and irradiation was positively correlated with the expression of COX-2 mRNA（ P 〈 0.01 ）. was observed from the dose-survival curve and the related parameters. The values of SER were 1.09 （ D0 ） or 1.11 （ D q ） in SHG-44 cells and 1.12 （ D0 ） or 3.01 （ Dq ） in SHG-4410Gy. Conclusions SHG--4410Gy cells are more radio-resistant, and one of the fundamental mechanisms might be the upregulation of COX-2 expression in protein and mRNA levels. Acetaminophen could enhance the radisensitivity of glioma cells, especially the surviving progeny from the irradiated SHG-44 cells.

关 键 词：放射增敏 COX-2 对乙酰氨基酚 胶质瘤 

分 类 号：R739.4[医药卫生—肿瘤]