Repository logo
  • English
  • 中文
  • Log In
    New user? Click here to register.Have you forgotten your password?
Repository logo
    Communities & Collections
    Research Outputs
    Fundings & Projects
    People
    Organizations
    Statistics
  • English
  • 中文
  • Log In
    New user? Click here to register.Have you forgotten your password?
  1. Home
  2. TMU Publications / 北醫出版品
  3. .博碩士學位論文
  4. .99學年度
  5. 探討KJ1樟芝萃取物抑制小膠質細胞活化之機轉及其於活體降低腦內出血傷害的效果
 
  • Details
Options

探討KJ1樟芝萃取物抑制小膠質細胞活化之機轉及其於活體降低腦內出血傷害的效果

Other Title
Investigation of the inhibitory mechanisms of KJ1 on microglia activation and intracerebral hemorrhage-induced injury in vivo
Type
thesis
Date Issued
2011-07-04
Author(s)
黃書賢
Advisor
蕭哲志
Subjects
系所名稱:醫學科學研究所
Description
學位別:碩士
語文別:中文
指導教授:蕭哲志
共同指導教授:
口試委員:顧記華;黃聰龍;陳炳常;黃玲玲
中文關鍵字:腦中風
Abstract
中文摘要
腦內出血是一種破壞性的神經系統疾病,其死亡率高且預後率差,到目前幾乎沒有效的藥物可以治療用。當血液滲入腦實質部形成血腫後,會導致水腫和活化神經膠細胞,如小膠質細胞,並分泌的各種前發炎細胞激素及神經致毒媒介,引起發炎反應並造成大腦組織的損傷。而藉由抑制神經膠細胞的過度活化,以降低因發炎物質產生造成的腦神經傷害。
本篇研究顯示,在脂多醣體刺激小膠質細胞實驗中,KJ1可以抑制iNOS及COX-2的蛋白表現。在訊息傳遞方面,KJ1可抑制Akt的磷酸化,以及在MAPK訊息傳遞路徑之ERK及JNK的磷酸化也有明顯抑制。
在活體實驗中,KJ1可以抑制膠原蛋白分解酶引起腦內出血所誘導的COX-2蛋白表現及MMP-9的活性;KJ1對腦內出血引起的腦水腫有改善作用,亦可減少神經細胞持續死亡,並改善神經行為。本篇另一藥物N96亦可以降低腦內出血所誘導MMP-9的活性。
上述結果顯示出在中樞神經系統中,KJ1可減少小微膠細胞受刺激後所產生的發炎物質,以改善其對腦內出血的傷害,以提供了神經細胞抗發炎之特性。
URI
https://203.71.86.71/handle/123456789/13589

Copyright Notice

● 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. Users must not use TMUIR for any illegal purposes.

● By utilising the platform, users are deemed to have fully accepted and understood all the regulations set out in this statement, relevant laws of the Republic of China, all international internet regulations, and usage conventions.

● TMUIR is committed to protecting the interests of copyright owners. If you believe that any material on this website infringes copyright, please contact our staff at libirtmu@gmail.com, and we will remove the work from the repository.

Built with DSpace-CRIS software - Extension maintained and optimized by 4Science

  • Cookie settings
  • Privacy policy
  • End User Agreement
  • Send Feedback