Taipei Medical University Institutional Repository:Item 987654321/5834
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 45422/58598 (78%)
Visitors : 2548232      Online Users : 332
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
    Home ‧ Login ‧ Upload ‧ Help ‧ About ‧ Administer Goto mobile version


    Please use this identifier to cite or link to this item: http://libir.tmu.edu.tw/handle/987654321/5834


    Title: Cinnamophilin 抑制腦血管內皮細胞凋亡之作用機轉探討
    Inhibitory Mechanisms of Cinnamophilin in Cerebral Endothelial Cell Apoptosis
    Authors: 魏苑茹
    Yuan-Ju Wei
    Contributors: 醫學研究所
    Keywords: 氧化態低密度脂蛋白
    腦血管內皮細胞
    Cinnamophilin
    活性氧分子
    ox-LDL
    Cerebral endothelial cell
    Cinnamophilin
    ROS
    Date: 2006
    Issue Date: 2009-09-11 15:44:24 (UTC+8)
    Abstract: 本論文主要探討由菲律賓樟樹 (Cinnamomum philippines) 中所分離出來的成分 cinnamophilin 抑制氧化態低密度脂蛋白 (oxidized low density lipoprotein; ox-LDL) 誘導小鼠腦血管內皮細胞 (cerebral endothelial cell; CEC) 死亡的機制研究。Cinnamophilin 以濃度相關方式抑制了 ox-LDL 所引發 CEC 的細胞凋亡現象以及caspase-9 和 caspase-3 的活化。但是cinnamophilin (10 µM) 並無法抑制 cytochrome c 或 Smac 由粒線體中釋放到細胞質中，更進一步，cinnamophilin 並不影響 ox-LDL 所引起的粒線體膜電位的減少。此外，cinnamophilin 能抑制 ox-LDL 造成的活性氧分子 (reactive oxygen species; ROS) 增加。GRP78 蛋白的表現代表其內質網壓力增加。Ox-LDL 以時間相關增加內質網壓力。Cinnamophilin 以濃度相關方式明顯抑制 ox-LDL 所引發 GRP78 蛋白質表現量增加。綜合以上，cinnamophilin 抑制 ox-LDL 誘導腦血管內皮細胞凋亡的機制可能是經由抑制 ROS 的增加、內質網壓力、caspase-9 和 caspase-3 的活化。因此 cinnamophilin 可能具有發展成為治療腦血管疾病的潛力。
    In this study, we attempted to evaluate the inhibitory mechanism of cinnamophilin, isolates from Cinnamomum philippinese, on oxidized low density lipoprotein (ox-LDL)- induced cerebral endothelial cell (CEC) death. Cinnamophilin inhibited the ox-LDL-induced CEC apoptosis and the activation of caspase-9 and caspase-3 in a concentration-dependent manner. However, cinnamophilin did not affect the release of cytochrome c and second-mitochondria-derived activator of caspase (Smac) from the mitochondria to the cytoplasm. Furthermore, cinnamophilin (10 µM) did not affect the ox-LDL-induced the loss of mitochondrial membrane potential. In addition, cinnamophilin concentration-dependently inhibited ox-LDL-induced production of reactive oxygen species (ROS). Ox-LDL increased endoplasmic reticulum (ER) stress, reflected by GRP78 expression, in a time-dependent manner. Cinnamophilin markedly inhibited ox-LDL-induced GRP78 expression in a concentration-dependent manner. Taken together, the inhibitory mechanism of cinnamophilin on ox-LDL-induced CEC apoptosis may be, at least in part, through suppression of ROS formation, ER stress, caspase-9, and caspase-3 activation. We conclude that cinnamophilin may have therapeutic potential in cerebrovascular diseases.
    Data Type: thesis
    Appears in Collections:[Graduate Institute of Medical Sciences] Dissertation/Thesis

    Files in This Item:

    File Description SizeFormat
    摘要.doc30KbMicrosoft Word152View/Open
    摘要.pdf56KbAdobe PDF191View/Open
    摘要.ppt132KbMicrosoft Powerpoint222View/Open
    摘要.ps287KbPostscript78View/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