Taipei Medical University Institutional Repository:Item 987654321/58712
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 45073/58249 (77%)
造访人次 : 2390078      在线人数 : 159
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 查询小技巧：
  • 您可在西文检索词汇前后加上"双引号"，以获取较精准的检索结果
  • 若欲以作者姓名搜寻，建议至进阶搜寻限定作者字段，可获得较完整数据
    •  进阶搜寻


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://libir.tmu.edu.tw/handle/987654321/58712


    题名: 異甘草素在體內及體外實驗中對於子宮內膜異位症的影響效應
    The effects of Isoliquiritigenin on endometriosis in vivo and in vitro
    作者: 許宜雯
    Hsu, Yi-Wen
    贡献者: 保健營養學研究所
    夏詩閔
    关键词: 子宮內膜異位;異甘草素;上皮間質轉化;發炎反應
    Endometriosis;Isoliquiritigenin;epithelial-mesenchymal transition;inflammatory
    日期: 2019-06-28
    上传时间: 2020-02-18 12:54:48 (UTC+8)
    摘要: 前言：子宮內膜異位 (Endometriosis) 的主要特徵為子宮內膜組織生長於正常位置外，如：卵巢、輸卵管及腹膜腔等，造成經痛、骨盆腔疼痛以及不孕等症狀。異甘草素 (Isoliquiritigenin, ISL) 為天然黃酮類化合物，主要由甘草根及蔥科植物中所萃取，先前研究指出異甘草素具有抗氧化、抗發炎、抗細胞增生以及抗腫瘤的效果。
    目的：以體內及體外實驗模式探討異甘草素對於子宮內膜異位症的影響效應。
    材料方法：使用人類子宮內膜異位細胞株End1/E6E7，介入雌激素與異甘草素，以MTT試驗分析細胞存活率，以傷口癒合試驗分析細胞轉移能力，以西方墨點法分析其上皮間質轉化相關蛋白表現量。24隻Balb/c雌性小鼠透過手術移植子宮組織至腹膜，並給予雌激素以誘導子宮內膜異位症的產生，期間以異甘草素或載體介入四週，並以超音波監測小鼠體內的子宮內膜異位組織，犧牲後以游標尺及秤測量異位組織體積及重量，並測定血液及異位組織中發炎因子的濃度，並以西方墨點法分析異位組織中上皮間質轉化以及細胞凋亡相關蛋白表現量。
    結果：介入異甘草素之End1/E6E7細胞，其細胞存活率及傷口癒合能力下降，也使細胞及異位組織中E-cadherin表現量上升、N-cadherin、Slug及Snail表現量下降。在體內實驗中，異甘草素抑制子宮內膜異位組織體積及重量，且減少血液及異位組織中發炎因子的濃度，並促進異位組織細胞凋亡的發生。
    結論：異甘草素具有抑制子宮內膜異位細胞的增生、轉移以及上皮間質轉化的作用、減少子宮內膜異位組織的體積及重量、降低血液及組織中血管內皮生長因子及發炎因子濃度、抑制異位組織上皮間質轉化的作用以及促進細胞凋亡，以達到改善子宮內膜異位症的效果。因此，異甘草素具有開發成改善子宮內膜異位症功能性配方之潛力。
    關鍵字：子宮內膜異位、異甘草素、上皮間質轉化、發炎反應
    Endometriosis is a common gynaecological disease characterized by the growth of uterine endometrial tissue outside the uterine cavity on ovarian, oviduct and the pelvic peritoneum. Isoliquiritigenin (ISL) is a natural flavonoid isolated from the root of licorice and shallot. ISL is reported to have several biological properties, including anti-oxidant, anti-inflammatory, anti-proliferation and anti-tumor. The study aimed to investigate effects of ISL on endometriosis in vivo and in vitro.
    Endometriosis cell End1/E6E7 were treated with ISL and β-estradiol. MTT assay were used to detect cell viability. The cell migration were evaluated by wound-healing assay. The expression of epithelial-to-mesenchymal transition (EMT) -related proteins were detected by Western blot. 24 female Balb/c mice surgically inducing endometriosis by uterine tissue transplantation into the abdominal cavity were treated with ISL or vehicle for 4 weeks. Lesions growth were subsequently analyzed by high-resolution ultrasound imaging. Inflammatory cytokines of serum and lesions were measured by ELISA. EMT-related proteins and apoptosis-related proteins of endometriotic lesions were detected by Western blot.
    It was observed the treatment of ISL inhibited the viability and migration of End1/E6E7. ISL treatment increased the expression of E-cadherin, decreased the expression of N-cadherin, Slug and Snail. In animal model, ISL treatment reduced the volume and weight of endometriotic lesions, decreased inflammatory cytokines of serum and lesions, inhibited EMT and induced apoptosis of lesions.
    ISL inhibited viability, migration and EMT-related proteins of End1/E6E7 cell, reduced the volume and weight of endometriotic lesions, inhibited inflammatory and EMT and induced apoptosis of lesions to improve endometriosis.
    Key words : Endometriosis, Isoliquiritigenin, epithelial-mesenchymal transition, inflammatory
    描述: 碩士
    指導教授：夏詩閔
    委員：黃翠琴
    委員：謝宗明
    数据类型: thesis
    显示于类别:[保健營養學系暨研究所] 博碩士論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    index.html0KbHTML36检视/开启


    检视Licence

    在TMUIR中所有的数据项都受到原著作权保护.

    TAIR相关文章

    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 ©   - 回馈