Taipei Medical University Institutional Repository:Item 987654321/4956
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 45073/58249 (77%)
Visitors : 2392084      Online Users : 162
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: http://libir.tmu.edu.tw/handle/987654321/4956


    Title: Eotaxin-1誘導人類軟骨細胞表現間質分解酵素-3(MMP-3)之可能訊息傳遞路徑探討
    Authors: 潘潔宜
    Contributors: 醫學檢驗暨生物技術學研究所
    Keywords: 骨關節炎
    趨化激素
    間質分解酵素
    Date: 2005
    Issue Date: 2009-09-10 17:21:47 (UTC+8)
    Abstract: 骨關節炎為一種常見的關節炎型式,其致病機轉目前仍不清楚,了解骨關節炎的致病過程對治療大有幫助,因此研究關節炎致病過程是很重要的研究課題。文獻指出趨化激素MCP-1、RANTES、IL-8、GRO-α與骨關節炎中軟骨細胞的分解及合成作用有密切關係。而Eotaxin是一種會趨化嗜酸性白血球的趨化激素,根據我們之前的研究顯示,使用IL-1β、TNF-α會刺激軟骨細胞增加Eotaxin-1的表現,而且Eotaxin-1也會誘導軟骨細胞分泌間質分解酵素MMP-3及MMP-13;其中MMP-3表現較明顯,證實Eotaxin-1具有參與調控軟骨間質分解的能力,但目前Eotaxin-1對於軟骨細胞訊息傳遞作用機制尚不清楚。根據結果顯示在MAPKase路徑方面,人類軟骨瘤細胞株SW-1353經Eotaxin-1刺激後,ERK1/2、p38有明顯被磷酸化的現象,JNK則無明顯變化,而在使用PD98059(MEK 抑制劑)及SB203580(p38抑制劑)後,可抑制由Eotaxin-1所誘導的MMP-3 mRNA的表現,由此可知在Eotaxin-1誘導軟骨細胞分泌MMP-3的訊息傳遞路徑中,ERK1/2及p38 MAPK的活化有參與在其中。此外,在IKK路徑方面,根據結果顯示, 使用Eotaxin-1刺激之下,IKKa/b、IkBa、NF-kB皆沒有被活化的情形,因此我們推測在軟骨細胞中,Eotaxon-1可能無法藉由活化IKK pathway進而誘導軟骨細胞分泌間質分解酵素MMP-3
    Data Type: thesis
    Appears in Collections:[ ] Dissertations/Theses

    Files in This Item:

    File Description SizeFormat
    google translate edition.doc48KbMicrosoft Word124View/Open
    摘要.doc24KbMicrosoft Word132View/Open
    摘要.pdf59KbAdobe PDF220View/Open
    摘要.ppt94KbMicrosoft Powerpoint148View/Open
    摘要.ps328KbPostscript103View/Open


    All items in TMUIR are protected by copyright, with all rights reserved.


    著作權聲明 Copyright Notice
    • 本平台之數位內容為臺北醫學大學所收錄之機構典藏,包含體系內各式學術著作及學術產出。秉持開放取用的精神,提供使用者進行資料檢索、下載與取用,惟仍請適度、合理地於合法範圍內使用本平台之內容,以尊重著作權人之權益。商業上之利用,請先取得著作權人之授權。

      The digital content on this platform is part of the Taipei Medical University Institutional Repository, featuring various academic works and outputs from the institution. It offers free access to academic research and public education for non-commercial use. Please use the content appropriately and within legal boundaries to respect copyright owners' rights. For commercial use, please obtain prior authorization from the copyright owner.

    • 瀏覽或使用本平台,視同使用者已完全接受並瞭解聲明中所有規範、中華民國相關法規、一切國際網路規定及使用慣例,並不得為任何不法目的使用TMUIR。

      By utilising the platform, users are deemed to have fully accepted and understood all the regulations set out in the statement, relevant laws of the Republic of China, all international internet regulations, and usage conventions. Furthermore, users must not use TMUIR for any illegal purposes.

    • 本平台盡力防止侵害著作權人之權益。若發現本平台之數位內容有侵害著作權人權益情事者,煩請權利人通知本平台維護人員([email protected]),將立即採取移除該數位著作等補救措施。

      TMUIR is made to protect the interests of copyright owners. If you believe that any material on the website infringes copyright, please contact our staff([email protected]). We will remove the work from the repository.

    Back to Top
    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback