English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 45422/58598 (78%)
造訪人次 : 2534334      線上人數 : 192
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/987654321/59452


    題名: 臺灣產植物成分及其對骨質新生活性研究 (1)
    The constituents from Taiwanese plant and their osteogenic activity (1)
    作者: 彭詩雯
    Peng, Shih-Wen
    貢獻者: 李美賢
    關鍵詞: 海州骨碎補;人類造骨細胞;腦源性神經滋養因子;骨質新生
    Davallia mariesii Moore ex Bak;human osteoblasts;osteogenic activity;brain-derived neurotrophic factor
    日期: 2015-07-14
    上傳時間: 2020-08-28 14:23:11 (UTC+8)
    摘要: 本研究乃採集海州骨碎補 (Davallia mariesii Moore ex Bak) 的根莖，以50%乙醇或二次水加熱迴流萃取，得到其乾燥萃取物，利用人類造骨細胞 (human osteoblasts) 進行活性評估：於MTT細胞存活率實驗中，發現二次水萃取物不具細胞毒性；在促進鹼性磷酸酶活性試驗和礦化染色試驗中，相較於控制組 (100%)，發現二次水萃取物對鹼性磷酸酶活性及礦化基質中鈣離子含量具有較好的促進效果 (分別為111.68±4.55%及130.23±4.29%)。因此將具活性之二次水萃取物進一步用多種管柱層析方式進行成分分離，得到三個化合物。經由理化及光譜相關數據分析以及文獻比對後，確認此三個化合物為一個amino acid及兩個glycoside。骨生成相關標誌物部分，過去研究發現，腦源性神經滋養因子 (BDNF) 基因上的phosSNP rs6265可調控造骨細胞的分化，並對骨密度產生影響。本研究發現隨著人類造骨細胞的分化與礦化，BDNF mRNA表現量逐漸增加。進一步利用人類造骨細胞進行此三個化合物之活性及其機轉探討：於MTT細胞存活率實驗中，發現均無細胞毒性；在促進骨生成活性與其機轉實驗中，發現三個化合物均對BDNF mRNA表現無顯著之促進效果，compound 1 可顯著促進骨骼成形蛋白-2 (BMP-2) 和骨唾液酸蛋白 (BSP) mRNA表現，而compound 2 具顯著促進礦化基質中鈣離子含量的能力，compound 3 則對BMP-2、BSP、第一型膠原蛋白 (Col-1) 和骨橋蛋白 (OPN) mRNA表現及礦化基質中鈣離子含量皆有顯著之促進效果。綜合上述結果，海州骨碎補具發展為骨質疏鬆藥物之潛力，而BDNF可能為具促進骨質新生活性的新標誌物。期望本論文之內容對未來骨質疏鬆的研究及其藥物的設計產生貢獻。
    In this study, we extracted the rhizoma of Davallia mariesii Moore ex Bak with ddH2O or 50% ethanol. Using cell viability assay, alkaline phosphatase (ALP) activity assay and mineralization staining assay, we evaluated the activities of the extracts in human osteoblasts (HOb). Our data showed that ddH2O extract of D. mariesii has better osteogenic activity than 50% ethanol extract. Hence, the ddH2O extract was further isolated and purified with a variety of columns. After bio-guided column chromatography, we obtain three known compounds. These compounds were identified as one amino acid and two glycosides. Brain-derived neurotrophic factor (BDNF) is an neurotrophin which can influence osteoblast differentiation and bone mass. We found that BDNF mRNA expression was upregulated gradually during differentiation and mineralization process in HOb. However, all of the three compounds didn’t regulate BDNF mRNA expression in HOb. Further, we investigate the effects of these compounds on cell viability, matrix mineralization and osteogenesis-related mRNA expression in HOb. The MTT assay showed that all of these compounds are nontoxic to HOb. Compound 1 could upregulate bone morphogenetic protein-2 (BMP-2) and bone sialoprotein (BSP) mRNA expression. Compound 2 and compound 3 significantly increased the calcium contents of the mineralized matrix in HOb, while compound 3 could also upregulate BMP-2, BSP, type I collagen (Col-1) and osteopontin (OPN) mRNA. The present results imply that Davallia mariesii has potential to be developed into osteoporosis drugs and BDNF is a new biomarker for bone research. Hoping that our study contributes to osteoporosis research and drug design in the future.
    描述: 碩士
    指導教授:李美賢
    委員:黃聰龍
    委員:徐鳳麟
    資料類型: thesis
    顯示於類別:[生藥學研究所] 博碩士論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    index.html0KbHTML69檢視/開啟


    檢視Licence

    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