English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 45422/58598 (78%)
造訪人次 : 2524680      線上人數 : 213
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/987654321/50818


    題名: 利用靜磁場誘導內毒素耐受性以降低脂多醣引發之腦部傷害
    Increment of endotoxin tolerance for reducing lipopolysaccharide induced brain injury by using static magnetic field
    作者: 楊博傑
    Yang, Po-Chieh
    關鍵詞: 內毒素耐受性;微膠細胞;靜磁場;腦部發炎反應;endotoxin tolerance;microglia;static magnetic field;inflammation of brain
    日期: 2012-01-16
    上傳時間: 2018-10-03 15:51:35 (UTC+8)
    摘要: 敗血症和神經退化性疾病都是由於發炎反應而造成腦部的傷害,目前均沒有有效的治療方式。因此以降低脂多醣造成全身的發炎反應,或是提升對於脂多醣的內毒素耐受性即成為抗感染治療的一個方向。可是要在腦部注射低劑量內毒素引發內毒素耐受性,其作用位置與注射劑量均很難控制。因此本研究探討在靜磁場(static magnet field, SMF)作用之下,對於接受內毒素注射的小鼠,其存活率和腦部病理切片是否有影響,此外並在有無靜磁場暴露之下,脂多醣對於BV-2微膠細胞的生長影響,及其誘導BV-2表現的細胞激素是否有差異。結果發現,靜磁場暴露能夠提升經脂多醣刺激小鼠的存活率,並減緩其小腦部位的發炎現象。而BV-2微膠細胞在受到靜磁場作用後,其生長數目會顯著低於未暴露磁場的細胞數量(p<0.05),且本研究發現暴露靜磁場的BV-2細胞,對於脂多醣誘導的毒殺作用,較之對照組亦有明顯的降低(p<0.05)。此外,以脂多醣刺激BV-2細胞的激素生成時,細胞會有類似內毒素耐受性的現象發生,尤其在暴露過靜磁場的細胞,其IL-6的生成量會明顯比未暴露靜磁場的細胞來的低(p<0.05)。這些結果均顯示,靜磁場可以誘導內毒素耐受性的發生,並因此降低脂多醣對於腦部的發炎反應以及傷害。

    The effective method for preventing brain-damage and neurodegeneration caused by inflammation is still limited. Down-expression of the lipopolysaccharide (LPS)-induced inflammatory cytokines and thus resulting in endotoxin tolerance was reported to be a new aspect for anti-infection treatment. However, since the dosage and action site are hard to control, endotoxin tolerance caused by low-dose LPS injection in brain tissue may induce side effects. The aim of this study was to test the hypothesis whether static magnetic field (SMF) can be a stimulation source for inducing endotoxin tolerance in brain tissue. This study, examined survival rate and brain tissue changes of LPS-challenged mice, pre-treated with or without SMF. In addition, the effects of SMF exposure on growth rate and cytokines expression of LPS-challenged BV-2 microglia cells were monitored. Our results showed that SMF pre-exposure had positive effects on the survival rate and histological outcomes of LPS-treated mice. Furthermore, SMF pre-exposure significantly increased IL-6 expression of BV-2 cell (p<0.05) and resulted in a significant reduction (p<0.05) of cytotoxicity in LPS treated cells. According to these results, although more advanced experiments are needed, it is reasonable to suggest that SMF has potential to be an alternative simulation source for inducing endotoxin tolerance in brain tissue.
    描述: 碩士
    指導教授-黃豪銘
    委員-蕭裕源
    委員-馮琮涵
    資料類型: thesis
    顯示於類別:[生醫材料暨組織工程研究所] 博碩士論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    index.html0KbHTML342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