中华放射医学与防护杂志
中華放射醫學與防護雜誌
중화방사의학여방호잡지
Chinese Journal of Radiological Medicine and Protection
2008年
5期
502-505
,共4页
周菊英%涂彧%徐晓婷%俞志英%秦颂兵%王利利%李莉%周乐源
週菊英%塗彧%徐曉婷%俞誌英%秦頌兵%王利利%李莉%週樂源
주국영%도욱%서효정%유지영%진송병%왕리리%리리%주악원
放射增敏%COX-2%对乙酰氨基酚%胶质瘤
放射增敏%COX-2%對乙酰氨基酚%膠質瘤
방사증민%COX-2%대을선안기분%효질류
Radiosensitization%COX-2%Acetaminopben%Glioma
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10 Gy 6 MV X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-4410 Gy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-4410 Gy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-4410 Gy中COX-2 mRNA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-4410 Gy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-4410 Gy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.
目的 探討對乙酰氨基酚聯閤放射對人噁性腦膠質瘤細胞2種細胞的放射增敏效應及其可能的機製.方法 以人噁性腦膠質瘤細胞株SHG-44及其接受10 Gy 6 MV X射線照射後的存活後代細胞SHG-4410 Gy為研究對象,採用免疫細胞化學和RT-PCR檢測 2株細胞COX-2的錶達,集落形成實驗測定對乙酰氨基酚對細胞的放射增敏作用.結果 HG-4410 Gy較SHG-44的放射敏感性低(P<0.01);免疫細胞化學染色SHG-44和SHG-4410 Gy細胞的胞質及胞膜均有COX-2蛋白的錶達,且後者明顯高于前者;RT-PCR檢測SHG-4410 Gy中COX-2 mRNA錶達水平明顯高于SHG-44細胞,與放射敏感性有顯著的相關性(r=0.976,P<0.01);對乙酰氨基酚聯閤放療分彆作用于SHG-44和SHG-4410 Gy細胞,與單純照射組相比,顯示瞭放射增敏作用,SHG-44細胞D0值和Dq值增敏比分彆為1.09和1.11,SHG-4410 Gy的SER分彆為1.12和3.01.結論 人噁性腦膠質瘤細胞株SHG-44及其照射存活後代細胞均有COX-2錶達,且對輻射耐受的存活後代細胞中COX-2明顯增高;對乙酰氨基酚可通過抑製COX-2的錶達增加人腦膠質瘤SHG-44細胞尤其是其照射後代細胞的放射敏感性.
목적 탐토대을선안기분연합방사대인악성뇌효질류세포2충세포적방사증민효응급기가능적궤제.방법 이인악성뇌효질류세포주SHG-44급기접수10 Gy 6 MV X사선조사후적존활후대세포SHG-4410 Gy위연구대상,채용면역세포화학화RT-PCR검측 2주세포COX-2적표체,집락형성실험측정대을선안기분대세포적방사증민작용.결과 HG-4410 Gy교SHG-44적방사민감성저(P<0.01);면역세포화학염색SHG-44화SHG-4410 Gy세포적포질급포막균유COX-2단백적표체,차후자명현고우전자;RT-PCR검측SHG-4410 Gy중COX-2 mRNA표체수평명현고우SHG-44세포,여방사민감성유현저적상관성(r=0.976,P<0.01);대을선안기분연합방료분별작용우SHG-44화SHG-4410 Gy세포,여단순조사조상비,현시료방사증민작용,SHG-44세포D0치화Dq치증민비분별위1.09화1.11,SHG-4410 Gy적SER분별위1.12화3.01.결론 인악성뇌효질류세포주SHG-44급기조사존활후대세포균유COX-2표체,차대복사내수적존활후대세포중COX-2명현증고;대을선안기분가통과억제COX-2적표체증가인뇌효질류SHG-44세포우기시기조사후대세포적방사민감성.
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 Gy 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(Dq) in SHG-44 cells and 1.12(D0)or 3.01 (Dq) in SHG-4410 Gy. Conclusions SHG-4410 Gy 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.