期刊文献+

白藜芦醇通过MyD88/TLR4/NF-kB信号通路诱导结肠癌细胞凋亡的机制 被引量:5

Mechanism of apoptosis of colon cancer cells induced by resveratrol through MYD88/TLR4/NF-KB signaling pathway
在线阅读 下载PDF
导出
摘要 目的探讨白藜芦醇通过MyD88/TLR4/NF-kB信号通路影响结肠癌细胞凋亡的机制。方法选取不同剂量白藜芦醇处理24 h后的结肠癌细胞,TUNEL法检测细胞凋亡率的变化,利用RT-PCR和Western blot检测白藜芦醇处理后结肠癌细胞MyD88/TLR4/NF-kB信号通路中关键信号分子的表达变化。结果中高剂量白藜芦醇处理结肠癌细胞系HT-29、sw480和LoVo后,细胞凋亡率显著上升;Bcl-2蛋白和mRNA含量表达下降,Bax、cleaved-Caspase 3蛋白和mRNA含量表达显著升高;细胞上清中VEGF蛋白表达明显降低;细胞中MyD88、TLR4、NF-kB和mRNA含量均明显降低。结论白藜芦醇可能通过MyD88/TLR4/NF-kB信号通路促进结肠癌细胞凋亡从而抑制肿瘤发生发展。 Objective To investigate the mechanism of apoptosis of colon cancer cells induced by resveratrol through MyD88/TLR4/NF-KB signaling pathway.Methods With different doses of resveratrol for 24 h,TUNEL assay was used to detect the apoptosis rate of colon cancer cells and Western blot and RT-PCR were employed to test the expression of key signal molecules in MyD88/TLR4/NF-kB signaling pathway.Results The apoptosis rates of HT-29,SW480 and LoVo significantly increased after treatment.The protein and mRNA levels of Bax and Cleaved Caspase 3 significantly increased and Bcl-2 was downregulated.The expression of VEGF protein in cell supernatant decreased significantly.MyD88,TLR4 and NF-KB were significantly down regulated(P<0.05).Conclusions Resveratrol may promote the apoptosis of colon cancer cells through MyD88/TLR4/NF-KB signaling pathway to inhibit the development of tumor.
作者 乔璐 杨艳 唐代诗 杜婷 顾勇 QIAO Lu;YANG Yan;TANG Daishi;DU Ting;GU Yong(Department of Gastroenterology,the Second Affiliated Hospital of Xi’an Jiaotong University,Xi’an 710004,China;Digestive System Department,the First Affiliated Hospital of AFMU,Xi’an 710032,China;Digestive System Department,Shaanxi Provincial Crops Hospital of Chinese People’s Armed Police Force,Xi’an 710054,China)
出处 《武警医学》 CAS 2022年第4期298-302,共5页 Medical Journal of the Chinese People's Armed Police Force
关键词 白藜芦醇 结肠癌 MYD88 TLR4 NF-KB resveratrol colon cancer MyD88 TLR4 NF-kB
  • 相关文献

参考文献4

二级参考文献32

  • 1郭云蔚,文卓夫,郑丰平.TLR2与TLR4在大肠癌组织中的表达特点[J].广东医学,2007,28(9):1435-1437. 被引量:8
  • 2Poltorak A,Smirnova I,Clisch R et al.Limits of a deletion spanning Tlr4 in C57BL/10ScCr mice.J Endotoxin Res,2000,6(1):51
  • 3Larvin M,McMahon MJ.APACHE-Ⅱ scores for assessment and monitoring of acute pancreatitis.Lancet,1989,2:201
  • 4Myriam AA,Matthew JF.Toll-like receptor:a family of pattern-recognition receptors in mammals.Genome Biology,2002,3(8):3 011
  • 5Hoshino K,Takeuchi O,Kawai T et al.Cutting edge:toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysacchaide:evidence for TLR4 as the Lps gene product.J Immunol,1999,162:3 749
  • 6Kiechl S,Lorenz E,Reindl M et al.Toll-like receptor 4 polymorphisms and atherogenesis.N Engl J Med,2002,347:185
  • 7China Medical Association.The clinical diagnosis and classification system for acute pancreatitis.Chinese Journal of surgery,1997,35(12):773
  • 8Isenmann R,Beger HG.Natural history of acute pancreatitis and the role of infection.Baillieres Best Pract Res Clin Gastroenterol,1999,13 (2):291
  • 9Medzhitov R,Preston-Hurlburt P,Janeway CA Jr.A human homologue of the Drosophila Toll protein signals activation of adaptive immunity.Nature,1997,388(6 640):394
  • 10Modlin RL,Brightbill HD,Godowski PJ.The toll of innate immunity on microbial pathogens.The New Eng Jour of Med,1999,340(23):1 834

共引文献6

同被引文献69

引证文献5

二级引证文献16

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