國家衛生研究院 NHRI:Item 3990099045/1490
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    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
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