期刊文献+

阿司匹林对人胶质母细胞瘤U87细胞系放射敏感性的影响 被引量:2

Effect of aspirin on radiosensitivity of human glioblastoma multiforme cell line U87
原文传递
导出
摘要 目的观察阿司匹林(ASA)对人胶质母细胞瘤U87细胞系放射敏感性的影响并探讨其可能机制。方法常规培养U87细胞,CCK-8法检测16、8、4、2、1、0.5mmol/LASA对细胞抑制率和1minol/LASA预处理对2、4、8Gy6MV—X射线单次照射后细胞抑制率的影响,计算ASA对这3种剂量射线的放射增敏比;选取1mmol/LASA和8Gy照射剂量进行实验,分为对照组、照射组、ASA组、ASA+照射组,流式细胞仪检测细胞凋亡和NF-κB的含量,激光共聚焦显微镜观察NF—κB的表达。结果与空白对照组比较,0.5、1mmol/LASA组细胞抑制率的差异无统计学意义(P〉0.05);ASA对8Gy射线的放射增敏比高于2、4Gy,差异有统计学意义(P〈0.05)。流式细胞仪检测结果显示,与照射组比较,ASA+照射组细胞凋亡率较高,NF-κB含量较低,差异均有统计学意义(P〈0.05)。激光共聚焦显微镜下观察显示,照射组细胞NF-κB在细胞质、细胞核均有表达,与ASA+照射组细胞比较表达较强。结论ASA可提高胶质母细胞瘤的放射敏感性,它可能通过抑制NF-κB的表达而增加由射线介导的胶质瘤细胞的凋亡,从而增强细胞对射线的反应。 Objective To observe the effect of aspirin (ASA) on radiosensitivity of human glioblastoma multiforme cell line U87, and explore its mechanism. Methods Routine culture of U87 cell line was performed; inhibitory effect of different doses of ASA (16, 8, 4, 2, 1 and 0.5 mmol/L) on the proliferation of U87 cells and the influence of 1 mmol/L ASA pretreatment on the proliferation of U87 cells after single fraction irradiation with 2, 4 and 8 Gy 6MV-X ray were detected with CCK-8; the radiation enhancement ratio (RER) of ASA on these 3 different radiation doses were calculated. We chose 1 mmol/L ASA and 8 Gy X-ray for further experiment; the U87 cells were divided into control group, radiation treatment group, ASA treatment group and radiation plus ASA treatment group; the changes of apoptosis rate and the level of NF-κB in each group were detected by flow cytometry (FCM), and the expression of NF-κB was observed by laser scanning confocal microscope. Results As compared with that of control group (not given ASA), the inhibitory effect on proliferation of U87 cells in 1 and 0.5 mmol/L ASA treatment groups was not significantly different (P〉0.05). The RER in radiation dose of 2, 4 and 8 Gy induced by ASA was (0.155±0.008), (0.205±0.017) and (0.392±0.024), respectively; 8 Gy treatment group had a significantly higher RER than 2 and 4 Gy treatment groups (/)〈0.05). FCM showed that ASA plus 8 Gy radiation treatment could increase the apoptosis rate of U87 from (7.74%±0.43%) to (12.58%±0.94%), however, it could decrease the level of NF-κB in U87 cells from (96.65%±2.79%) to (77.06%±2.89%); significant differences between control group and ASA plus radiation treatment group were noted (P〈0.05). Laser scanning confocal microscope showed that the expression of NF-κB mainly appeared in the cytoplasm ad nucleus after irradiation, and its expression could be inhibited by ASA. Conclusion ASA could increase the radiosensitivity of U87 cells by inhibiting the expression of NF-κB to increase the apoptosis of glioma cells.
出处 《中华神经医学杂志》 CAS CSCD 北大核心 2011年第11期1110-1114,共5页 Chinese Journal of Neuromedicine
基金 国家自然科学基金海外青年学者合作研究基金(30628018) 广东省医学科学技术研究基金(A2008427)
关键词 胶质母细胞瘤 阿司匹林 放射敏感性 Glioblastoma multiforme Aspirin Radiosensitivity
  • 相关文献

参考文献11

  • 1Mao XG, Zhang X, Zhen HN. Progress on potential strategies to target brain tumor stem cells[J]. Cell Mol Neurobiol, 2009, 29(2): 141-155.
  • 2Mayo M, Baldw in AS. The transcription factor NF-KB: Control ofoncogenesis and cancer therapy resistance [J]. Biochim Biophys Acta, 2000, 1470(2): 55-62.
  • 3Thoms HC, Dunlop MG, Stark LA, et al. P38-mediated inactivation of cyclin D1/ cyclin-dependent kinase 4 stimulates nucleolar translocation of RelA and apoptosis in colorectal cancer cells [J]. Cancer Res, 2007, 67(4): 1660-1669.
  • 4Kim KY, Seol JY, Jeon GA, et al. The combined treatment of aspirin and radiation induces apoptosis by the regulation of bcl-2 and caspase23 in human cervical cancer cell[J]. Cancer Lett, 2003, 89(2): 157-166.
  • 5Jacobs EJ, Thum MJ, Bain EB, et al. A large cohort study of long-term daily use of adult 2st rength aspirin and cancer incidence [J]. J Natl Cancer Inst, 2007, 99(8): 608-615.
  • 6Karin M, Cao Y, Greten FR, et al. NF-kappaB in cancer: from innocent bystander to major culprit Nat Rev[J]. Cancer, 2002, 2(4): 301-310.
  • 7Ho E, Ames BN. Low intracellular zinc induces oxidative DNA damage, disruptsp53, NFkappaB, andAP1 DNAbinding, and affects DNA repair in a rat glioma cell line[J]. Proc Natl Acad Sci USA, 2002, 99(26): 16770-16775.
  • 8Cuevas P, Diaz-Gonzalez D, Dujovny M. Glioma cell-associated sustained activation of the transcription factor, nuclear factor-kappa B, was inhibited by neomycin [J]. Neurol Res, 2003, 25 (3): 271-274.
  • 9Campbell A, Yang EY, Tsai-Turton M, et al. Pro-inflammatory effects of aluminum in human glioblastoma cells [J]. Brain Res, 2002, 933(1): 60-65.
  • 10Ding GR, Honda N, Nakahara T, et al. Radiosensitization by inhibition of IkappaB-alpha phosphorylation in human glioma cells [J]. Radiat Res, 2003, 160(2): 232-237.

同被引文献23

  • 1蔡玉亮,崔森,王红心.慢性高原病患者骨髓单个核细胞Caspase-3表达研究[J].现代临床医学,2011,37(5):333-334. 被引量:4
  • 2Krajewska M, Krajewski S, Epstein J I, et al. Immunohistoche- mical analysis of Bcl 2,Bax, Bcl-X, and mcl-1 expression in prostate cancers [J]. Am J Pathol, 1996,148(5) : 1567-1576.
  • 3Peter M E, Heufelder A E, Hengartner M O. Advances in apoptosis research [J]. Proc Natl Acad Sci USA, 1997,94(24) : 12736-12737.
  • 4Ren ZG, Zhao JD, Gu K, et al. Three-dimensional conformal radiation therapy and intensity-modulated radiation therapy combined with transcatheter arterial chemoembolization for locally advanced hepatocellular carcinoma: an irradiation dose escalation study[J]. Int J Radiat Oncol Biol Phys, 2011, 79(2):496-502.
  • 5Gao B, Wang H, Lafdil F, et al. STAT proteins-key regulators of anti-viral responses, inflammation, and tumorigenesis in the liver[J]. J Hepatol, 2012, 57(2):430-441.
  • 6Frank DA. STAT3 as a central mediator of neoplastic cellular transformation[J]. Cancer Lett, 2007, 51(2):199-210.
  • 7Yu H, Jove R. The STATs of cancer—new molecular targets come of age[J]. Nat Rev Cancer, 2004, 4(2):97-105.
  • 8Siveen KS, Sikka S, Surana R, et al. Targeting the STAT3 signaling pathway in cancer: role of synthetic and natural inhibitors[J]. Biochim Biophys Acta, 2014, 1845(2):136-154.
  • 9Calvisi DF, Ladu S, Gorden A, et al. Ubiquitous activation of Ras and Jak/Stat pathways in human HCC[J]. Gastroenterology, 2006, 130(4):1117-1128.
  • 10He G, Dhar D, Nakagawa H, et al. Identification of liver cancer progenitors whose malignant progression depends on autocrine IL-6 signaling[J]. Cell, 2013, 155(2):384-396.

引证文献2

二级引证文献10

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部