國家衛生研究院 NHRI:Item 3990099045/3617
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12145/12927 (94%)
造访人次 : 853993      在线人数 : 1386
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/3990099045/3617


    题名: COX-2 and iNOS are critical in advanced glycation end product-activated chondrocytes in vitro
    作者: Huang, CY;Hung, LF;Liang, CCT;Ho, LJ
    贡献者: Institute of Cellular and Systems Medicine
    摘要: Eur J Clin Invest 2009; 39 (5): 417-428AbstractBackground The advanced glycation end products (AGEs) accumulate in joints of osteoarthritis patients. This study aimed to investigate the roles of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) pathways in AGE-mediated cartilage damage. Materials and methods Methylglyoxal-modified albumin was used as the source of AGE. Porcine and human chondrocytes were prepared from the joint cartilage of pigs and osteoarthritis patients. The activation of COX-2, iNOS, nuclear factor-kappaB (NF-B), activator protein-1 (AP-1) and protein kinases was determined by Western blotting, kinase assay, electrophoretic mobility shift assay (EMSA) or transfection assay. Prostaglandin E2 (PGE2) and NO concentrations were determined by enzyme-linked immunosorbent assay (ELISA) and Griess reaction respectively. The enzymatic activity of COX was determined by measuring the conversion of arachidonic acid to PGE2. The release of sulphated glycosaminoglycan and the intensity of Safranin O staining were used to measure cartilage degradation. Results AGE potently induced COX-2-PGE2 and iNOS-NO activation in porcine and human chondrocytes. Meanwhile, the upstream molecules regulating COX-2/iNOS activation, such as AP-1, NF-B, extracellular signal regulated protein kinase (ERK) and c-jun N-terminal kinase (JNK), were activated by AGE. Although AGE could not activate p38 directly, by measuring COX enzyme activity, the inhibition of p38 resulted in suppressing AGE-induced conversion of arachidonic acid to PGE2. Furthermore, successful blockage of either COX-2 or NOS activity significantly reduced AGE-mediated proteoglycan release and cartilage degradation. Conclusions This study highlights the significance of COX-2 and iNOS pathways in AGE-mediated OA pathogenesis and their potential as therapeutic targets that are beyond pain killing for OA treatment.
    日期: 2009-05
    關聯: European Journal of Clinical Investigation. 2009 May;39(5):417-428.
    Link to: http://dx.doi.org/10.1111/j.1365-2362.2009.02106.x
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0014-2972&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000264822100010
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=63849158704
    显示于类别:[何令君] 期刊論文
    [梁春金(2004-2009)] 期刊論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    SCP63849158704.pdf420KbAdobe PDF1000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