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(教師升等著作 / 教學實踐 / 學位論文)
  3. .博碩士學位論文
  4. .99學年度
  5. Ellagic acid抑制血小板凝集作用之機轉探討
 
  • Details
Options

Ellagic acid抑制血小板凝集作用之機轉探討

Other Title
Mechanisms involved in the antiplatelet activity of ellagic acid
Type
thesis
Date Issued
2011-06-23
Author(s)
林俐君
Advisor
許準榕
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:許準榕
共同指導教授:
口試委員:蕭哲志;許銘仁;黃德富;顏茂雄
中文關鍵字:鞣花酸
Abstract
Ellagic acid為一種多酚類(polyphenols)的抗氧化物質,存在於一些蔬菜(vegetables)或植物的果實(fruits)中,例如核桃、胡桃、草莓、石榴、枸杞、葡萄等,目前有許多體外及動物模式研究指出ellagic acid有抑制發炎反應(anti-inflammatory)、抗氧化(anti-oxidant)及抗凝血(anti-coagulatory)的作用,但是關於ellagic acid對於血小板功能的影響並未被明確的探討,因此本篇研究主要是想探討ellagic acid對於血小板活化過程的影響以及其訊息傳遞方面的抑制機轉。由本研究的實驗結果顯示,ellagic acid在濃度50-80 uM,對於collagen引起的人類血小板凝集反應及ATP的釋放會有抑制的作用。而測定血小板內PKC活性的實驗中發現ellagic acid (80 uM)可以顯著地抑制由collagen所活化的47 kDa和PLCr2蛋白質磷酸化,且呈現濃度相關的抑制作用;ellagic acid (50-80 uM)也會明顯抑制由collagen所活化的Akt磷酸化;而對於p38 MAPK、ERK1/2及JNK1的磷酸化,ellagic acid (50-80 uM)也有意義的抑制作用。由上述的實驗結果可以証實,ellagic acid抑制血小板活性的作用會涉及下列路徑:ellagic acid會經由調節PLCr2-PKC這條路徑來進一步抑制鈣離子的流動;此外,ellagic acid也會經由抑制hydroxyl radical (OH‧)的產生來降低MAPKs和Akt磷酸化的程度。此研究結果證實ellagic acid除了擔任抗發炎的功能之外,對於血小板凝集也有抑制的作用,因此未來可以當作一個有效的研究工具,以協助治療心血管方面之相關疾病。
URI
https://203.71.86.71/handle/123456789/13568

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