期刊文献+

阿司匹林对Jurkat细胞体外作用的实验研究 被引量:1

The experimental research of aspirin effect on Jurkat cells
在线阅读 下载PDF
导出
摘要 目的:探讨非甾体类抗炎药阿司匹林对存在有β-连环素异常表达的T淋巴细胞白血病Jurkat细胞株的作用及机制。方法:MTT法观察阿司匹林对Jurkat细胞的增殖抑制作用,流式细胞仪(FCM)检测阿司匹林对Jurkat细胞细胞周期分布的影响。实时荧光定量RT-PCR法分析经不同浓度的阿司匹林处理后的Jurkat细胞β-连环素及CyclinD1基因的表达水平的改变。结果:阿司匹林呈剂量依赖性抑制Jurkat细胞的增殖,72h半数抑制浓度为1.78mmol/L;随浓度增加,CyclinD1基因及蛋白的表达水平均下调。结论:非甾体类抗炎药阿司匹林可能通过影响Wnt信号通路调节某些细胞周期相关基因的表达,将Jurkat细胞阻滞于G0/G1期,从而抑制白血病细胞株Jurkat的增殖。 Objective:To explore the effects of aspirin on proliferation of T-acute lymphoblastic leukemia cells lines Jurkat in vitro. Method:Jurkat cells were treated with aspirin at different concentrations in culture. Growth inhibition was detected by MTT assay, The changed cell cycles distribution of Jurkat cells induced by aspirin was analysed by flow cytometry. The expression of β-catenin and CyclinD1 were detected by SYBR Green Ⅰ -based real -time quantitative RT-PCR. Result: Aspirin treatment caused a dose-dependent inhibition of J urkat cell proliferation, with a 72 h IC50 of 1.78 mM. Aspirin could commit Jurkat cells to G0/G1 phase arrest. At the same time, aspirin treatment induced a decrease in the expression level of CyclinD1 mRNA and expression level of CyclinD1 protein. Conclusion: Non-steroidal anti-inflammatory drugs aspirin treatment could inhibit proliferation of Jurkat cells by decreasing abnormal expression of CyclinD1.
出处 《临床血液学杂志》 CAS 2008年第1期35-38,共4页 Journal of Clinical Hematology
关键词 细胞株 JURKAT 基因 阿司匹林 细胞增殖 细胞周期 Cell line Gene Aspirin Cell proliferation Cell cycle
  • 相关文献

参考文献11

  • 1DIHLMANN S, SIERMANN A, VON KNEBEL DOEBERITA M. The nonsteroidal anti-inflammatory drugs aspirin and indomethacin attenuate beta-carenin/TCF-4 signaling [J]. Oncogene, 2001,20 : 645 - 653.
  • 2HARRIS R E, BEEBE-DONK J, DOSS H, et al. Aspirin,ibuprofen and other non-steroidal anti-inflammatory drugs in cancer prevention: a critical review of non-selective COX-2 blockade (review) [J]. Oncol Rep, 2005,13 : 559-- 583.
  • 3HUSAIN S S,SZABO I L,TAMAWSKI A S. NSAID inhibition of G1 cancer growth: clinical implications and molecular mechanisms of action[J]. Am J Gastroenterol, 2002,97:542 -- 553.
  • 4MARX J. Anti-inflammatories inhibit cancer growth, but how[J] ? Science, 2001,291:581 -- 582.
  • 5TAKETO M M. Cyclooxygenase-2 inhibitors in tumorigenesis(Part Ⅰ)[J]. J Natl Cancer Inst (Bethesda),1998,90:1529-- 1536.
  • 6TAKETO M M. Cyclooxygenase-2 inhibitors in tumorigenesis(Part Ⅱ)[J]. J Natl Cancer Inst (Bethesda), 1998,90 : 1609-- 1620.
  • 7MARX J. Anti-inflammatories inhibit cancer growth, but how[J] ? Science, 2001,291 : 581 -- 582.
  • 8ZHANG X, MORHAM S G, LANGENBACH R, et al. Malignant transformation and antineoplastic actions of nonsteroidal anti-inflammatory drugs (NSAIDs) on cyclooxygenase-null embryo flbroblasts[J]. J Exp Med,1999,190:451--459.
  • 9DIHLMANN S,SIERMANN A,VON KNEBEL DOEBERITZ M. The nonsteroidal anti-inflammatory drugs aspirin and indomethacin attenuate 13-catenin/ TCF-4 signaling[J]. Oncogene, 2001,20 : 645 -- 653.
  • 10GERMANN A, DIHLMANN S, HERGENHAHN M,et al. Expression profiling of CC531 colon carci- noma cells reveals similar regulation of beta-catenin target genes by both butyrate and aspirin[J]. Int J Cancer, 2003,106 : 187-197.

同被引文献4

引证文献1

二级引证文献2

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