國家衛生研究院 NHRI:Item 3990099045/1490
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12145/12927 (94%)
造访人次 : 855035      在线人数 : 953
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 查询小技巧：
  • 您可在西文检索词汇前后加上"双引号"，以获取较精准的检索结果
  • 若欲以作者姓名搜寻，建议至进阶搜寻限定作者字段，可获得较完整数据
    •  进阶搜寻
    主页 ‧ 登入 ‧ 上传 ‧ 说明 ‧ 关于NHRI ‧ 管理 到手机版


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/1490


    题名: The inhibition of TNF-alpha-induced E-selectin expression in endothelial cells via the JNK/NF-kappa B pathways by highly N-acetylated chitooligosaccharides
    其它题名: The inhibition of TNF-α-induced E-selectin expression in endothelial cells via the JNK/NF-κB pathways by highly N-acetylated chitooligosaccharides
    作者: Lin, CW;Chen, LJ;Lee, PL;Lee, CI;Lin, JC;Chiu, JJ
    贡献者: Division of Medical Engineering Research
    摘要: Chitooligosaccharides (COS) have been shown to regulate various cellular and biological functions. However, the effect of COS on inflammatory responses of the cells remains unclear. We investigated the regulatory effect of highly N-acetylated COS (NACOS) on tumor necrosis factor-alpha (TNF-alpha)-induced endotheliat cell (EC) E-selectin expression, which is crucial for leukocyte recruitment. ECs were kept as controls or pre-treated with NACOS for different times, and then stimulated with TNF-alpha for 4h. The results show that pre-treating ECs with NACOS inhibited the TNF-alpha-induced E-selectin expression in a dose- and time-dependent manner. This NACOS-mediated inhibition in E-selectin expression was regulated at the transcriptional level, but not due to changes in mRNA stability. Stimulation of ECs with TNF-a-induced rapid increases in the phosphorylation of their mitogen-activated protein kinases (MAPKs) [extracellular signal-regulated kinase (ERK), c-Jun-NH2-terminal kinase (JNK), and p38 MAPK]; the inhibitor for JNK (i.e., SP600125), but not those for ERK (i.e., PD98059) and p38 MAPK (i.e., SB203580), attenuated this TNF-alpha-induced E-selectin expression. Pre-treating ECs with NACOS inhibited the TNF-alpha-induced JNK activation, suggesting that JNK was involved in the inhibitory effect of NACOS on TNF-alpha-induced E-selectin expression. Pre-treating ECs with NACOS inhibited the TNF-a-induced p65 and p50 mRNA expressions. Gel shifting and chromatin immunoprecipitation assays showed that NACOS blocked the TNF-a-induced increases in the binding activity and in vivo promoter binding of nuclear factor-kappa B (NF-kappa B) in ECs. Our findings provide a molecular mechanism by which NACOS inhibit TNF-o(-induced E-selectin expression in ECs, and a basis for using NACOS in pharmaceutical therapy against inflammation. (c) 2006 Elsevier Ltd. All rights reserved.
    关键词: Engineering, Biomedical;Materials Science, Biomaterials
    日期: 2007-03
    關聯: Biomaterials. 2007 Mar;28(7):1355-1366.
    Link to: http://dx.doi.org/10.1016/j.biomaterials.2006.11.006
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0142-9612&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000243773200004
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33845658213
    显示于类别:[裘正健] 期刊論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    000243773200004.pdf726KbAdobe PDF705检视/开启


    在NHRI中所有的数据项都受到原著作权保护.

    TAIR相关文章

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回馈