English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 45422/58598 (78%)
造訪人次 : 2537237      線上人數 : 230
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜尋範圍 查詢小技巧:
  • 您可在西文檢索詞彙前後加上"雙引號",以獲取較精準的檢索結果
  • 若欲以作者姓名搜尋,建議至進階搜尋限定作者欄位,可獲得較完整資料
  • 進階搜尋
    請使用永久網址來引用或連結此文件: http://libir.tmu.edu.tw/handle/987654321/8269


    題名: Herbal Remedy Magnolol Suppresses IL-6-Induced STAT3 Activation and Gene Expression in Endothelial Cells,
    作者: 陳識中
    SC Chen;YL Chang;DL Wang;JJ Cheng
    貢獻者: 醫學系內科學科
    關鍵詞: Magnolol;endothelial cells;STAT3;ICAM-1;cyclin D1
    日期: 2006
    上傳時間: 2009-10-06 12:20:09 (UTC+8)
    摘要: Magnolol (Mag), an active constituent isolated from the Chinese herb Hou p’u (Magnolia officinalis)
    has long been used to suppress inflammatory processes. Chronic inflammation is well known to
    be involved in vascular injuries such as atherosclerosis in which interleukin (IL)-6 may participate.
    Signal transducer and activator of transcription protein 3 (STAT3), a transcription factor involved
    in inflammation and the cell cycle, is activated by IL-6. In this study, we evaluated whether Mag can
    serve as an anti-inflammatory agent during endothelial injuries. The effects of Mag on IL-6-induced
    STAT3 activation and downstream target gene induction in endothelial cells (ECs) were examined.
    Pretreatment of ECs with Mag dose dependently inhibited IL-6-induced Tyr705 and Ser727
    phosphorylation in STAT3 without affecting the phosphorylation of JAK1, JAK2, and ERK1/2.
    Mag pretreatment of these ECs dose dependently suppressed IL-6-induced promoter activity of
    intracellular cell adhesion molecule (ICAM)-1 that contains functional IL-6 response elements
    (IREs). An electrophoretic mobility shift assay (EMSA) revealed that Mag treatment significantly
    reduced STAT3 binding to the IRE region. Consistently, Mag treatment markedly inhibited ICAM-1
    expression on the endothelial surface. As a result, reduced monocyte adhesion to IL-6-activated ECs
    was observed. Furthermore, Mag suppressed IL-6-induced promoter activity of cyclin D1 and
    monocyte chemotactic protein (MCP)-1 for which STAT3 activation plays a role. In conclusion, our
    results indicate that Mag inhibits IL-6-induced STAT3 activation and subsequently results in the
    suppression of downstream target gene expression in ECs. These results provide a therapeutic basis
    for the development of Mag as an anti-inflammatory agent for vascular disorders including
    atherosclerosis
    關聯: British J Pharmacol, 2006, 148, 226-232. (* correspondence).(148):226-232.
    資料類型: article
    顯示於類別:[內科學科] 期刊論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    one31.pdf299KbAdobe PDF48檢視/開啟
    摘要.pdf33KbAdobe PDF64檢視/開啟


    在TMUIR中所有的資料項目都受到原著作權保護.

    TAIR相關文章

    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 ©   - 回饋