期刊文献+

二烯丙基二硫与硼替佐米联合应用诱导成神经细胞瘤细胞凋亡及活性氧的生成

Apoptosis and ROS production induced by diallyl disulfide in combination with bortezomib in neuroblastoma cells
下载PDF
导出
摘要 目的:探讨二烯丙基二硫(DADS)与硼替佐米(bortezomib)联合应用诱导人成神经细胞瘤SH—SY5Y细胞凋亡以及活性氧(ROS)的变化。方法:分别以DADS、硼替佐米单药和联合用药处理成神经瘤细胞SH—SY5Y细胞株,采用四甲基偶氮唑盐(MTT)比色法测定对细胞增殖的影响,Hoechst-33528染色观察细胞凋亡形态,流式细胞术检测细胞凋亡以及细胞内ROS的变化。结果:DADS和硼替佐米联合应用可使SH—SY5Y细胞的凋亡急剧增加,它们的联合应用还使细胞内ROS的生成比任何单一用药都多。结论:硼替佐米可促进DADS诱导SH—SY5Y细胞发生凋亡,ROS的产量增加可能在其中发挥了重要作用。 To explore the apoptosis of neuroblastoma cells and the change of ROS induced by diallyl disulfide (DADS) in combination with bortezmib. Methods: Neuroblastoma SH-SYSY cells were treated with DADS, bortezomib and DADS plus bortezomib. The cell viability was detected by methyl thiazolyl tetrazolium (MTT), and Hoechst-33528 stainning was employed to observe the apoptosis morphology. The production of ROS and the apoptotic rate of cells were measured by a flow cytometry method. Results: The combination of DADS and bortezomib increased the apoptosis of neuroblastoma cells, and their combination produced more ROS than when either was used alone. Conclusion: Bortezomib can facilitate the apoptosis of neuroblastoma induced by DADS; The enhanced production of ROS plays an important role during this process.
出处 《解剖学杂志》 CAS CSCD 北大核心 2011年第3期354-357,387,共5页 Chinese Journal of Anatomy
基金 山东省自然科学基金(2009ZRB01288) 滨州医学院科研计划与科研启动基金(BY2009KJlO)
关键词 活性氧 硼替佐米 二烯丙基二硫 成神经细胞瘤 细胞凋亡 reactive oxygen species bortezomib diallyl disulfide neuroblastoma cell apoptosis
  • 相关文献

参考文献8

  • 1George R E, Li S, Medeiros-Nancarrow C, et al. High-risk neu- roblastoma treated with tandem autologous peripheral-blood stem cell-supported transplantation: long-term survival update[J]. J Clin Oncol, 2006,24(18) : 2891-2896.
  • 2Filomeni G, Aquilano K, Rotilio G, et al. Reactive oxygen spe- cies- dependent c-Jun NHz-terminal Kinase/c-Jun signaling cas- cade mediates neuroblastoma cell death induced by diallyl disulfide [J]. Cancer Res, 2003,63(18) :5940-5949.
  • 3Utecht K N, Kolesar J. Bortezomib.. A novel chemotherapeutic a- gent for hematol-ogic malignancies [J ]. Am J Health Syst Pharm, 2008,65(13) :1221-1231.
  • 4Orlowski R Z. The ubiquitin proteasome pathway from bench to bedside [J] Hematology, 2005:220-225.
  • 5Valentiner U, Haane C, Nehmann N, et al. Effects of borte- zomib on human neuroblastoma cells in vitro and in a metastatic xenograft model [J]. Anticancer Res, 2009,29(4) : 1219-1225.
  • 6Pagnan G, Paolo D D, Carosio R, et al. The combined therapeu- tic effects of bortezomib and fenretinide on neuroblastoma cells in- volve endoplasmic reticulum stress response [J]. Clin Cancer Res, 2009,15 (4) : 1199-1209.
  • 7Sasazuki T, Okazaki T, Tada K, et al. Genome wide analysis of TNF-inducible genes reveals that antioxidant enzymes are induced by TNF and responsible for elimination of ROS [J]. Mol Immu-nol, 2004,41(5):547-551.
  • 8Zhang Y, Chen F. Reactive oxygen species (ROS), troublemak- ers between nuclear factor-cB (NF-KB) and c-Jun NH2-terminal kinase (JNK) [J]. Cancer Res, 2004,64(6):1902-1905.

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