English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 45422/58598 (78%)
造訪人次 : 2514292      線上人數 : 196
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/987654321/5521


    題名: Meclizine 誘發人類直腸腫瘤細胞(COLO 205)細胞週期停滯及細胞凋亡之分子機制研究
    Studies on the molecular mechanisms of Meclizine-induced cell cycle arrest and apoptosis in human colon adenocarcinoma cells
    作者: 林俊昌
    Jiunn-Chang Lin
    貢獻者: 醫學研究所
    關鍵詞: 細胞凋亡
    細胞週期停滯
    人類直腸腫瘤細胞
    meclizine
    apoptosis
    cell cycle arrest
    human colorectal cell
    日期: 2003
    上傳時間: 2009-09-11 15:34:50 (UTC+8)
    摘要: Meclizine (以下簡稱Mec)是一種用來治療頭暈和暈眩的用藥，為抗組織胺藥物的一種。在藥物與細胞的交互作用之中，我們發現Mec會讓人類直腸腫瘤細胞COLO 205誘發細胞凋亡現象。在人類直腸腫瘤細胞COLO 205中，以不同濃度的Mec處理細胞24小時後，觀察到細胞在50mM以上濃度有讓細胞走向細胞凋亡dose-dependent的情形。同時，在顯微鏡之下觀察可以看到隨著Mec藥物濃度增加，細胞數目隨之減少。在流式細胞儀的分析之中，也可以看到處於G0/G1 phase的細胞比例會因著Mec的作用而增加。在以西方墨點法分析各種相關蛋白質的變化之後，關於細胞週期停滯方面我們觀察到p53與p21蛋白在Mec作用之後都會升高，而CDK2和CDK4的活性則受到抑制，這就是Mec造成細胞週期停滯的機轉。在引起細胞凋亡方面，我們看到Mec可以dose-dependently造成以下結果: p53蛋白表現量增加，Bcl-2蛋白表現量減少，Bad蛋白表現量不變，cytochrome C由粒線體釋放到細胞質中，AIF由粒腺體進入細胞核中，Apaf-1蛋白表現量不變，Caspase 9，Caspase 8，Caspase 3活化，PARP被degrade。根據這些結果和文獻的探討，我們提出一個模式圖來解釋Meclizine引起COLO 205細胞走向細胞凋亡和細胞週期停滯的分子機轉。
    Meclizine, a kind of histamine H1 antagonist, has been used in the treatment of motion sickness and vertigo. In studying the interaction of drugs and cancer cell lines, we have found that meclizine dose-dependently induced apoptosis in COLO 205 cells. By DNA ladder assay, we demonstrated that DNA ladder appeared with meclizine treatment in COLO 205 cells if dosage larger than 50 μM. Besides, we observed that cell numbers decreased dose-dependently after treatment with meclizine in COLO 205 cells. By flow cytometry, we noticed that the percentage of COLO 205 cells in G0/G1 phase increased dose-dependently. We analyzed the change of associated protein by Western blot. About cell cycle arrest, p53 and p21 were upregulated after treatment with meclizine and resulted in decreasing CDK2 and CDK4 kinase activity. About apoptosis, meclizine induces upregulation of p53, downregulation of Bcl-2, release of cytochrome C into cytosol from mitochondria, translocation of AIF to the nucleus from mitochondria, and activation of caspase 3, caspase 8, and caspase 9. According to these data and concepts from references, we propose a flowchart to explain the possible mechanism of meclizine-induced apoptosis and cell cycle arrest in COLO 205 cell.
    資料類型: thesis
    顯示於類別:[醫學科學研究所] 博碩士論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    摘要.doc31KbMicrosoft Word116檢視/開啟
    摘要.pdf113KbAdobe PDF195檢視/開啟
    摘要.ppt121KbMicrosoft Powerpoint150檢視/開啟
    摘要.ps563KbPostscript61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