請用此 Handle URI 來引用此文件:
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/50907
標題: | IL-1β經由NOX4誘導人類牙齦纖維母細胞CC趨化因子20生成 NADPH Oxidase 4 Mediates IL-1β induced CCL20 in Human Gingival Fibroblasts |
作者: | Lih-Jia Huang 黃俐嘉 |
指導教授: | 郭彥彬 |
關鍵字: | 牙周病,人類牙齦纖維母細胞,IL-1β,CCL20,過氧化物,NOX4,薑黃素, Periodontitis,Human gingival fibroblast,IL-1β,CCL20,ROS,NOX4,Curcumin, |
出版年 : | 2016 |
學位: | 碩士 |
摘要: | Periodontal diseases have a high prevalence in Taiwan. The primary cause of periodontitis is poor or ineffective oral hygiene, which leads to the accumulation of bacterial matrix, called dental plaque. Subgingival micro-organisms would deposit endotoxin and cause further inflammation in the gum tissues and progressive bone loss. During the inflammation process, a lot of cytokines will increases in expression. One of them is Interleukin-1β (IL-1β). IL-1βhas the ability to induce Chemokine (C-C motif) ligand 20 (CCL20), and CCL20 can attract T helper cell to the inflamed gingival tissue, causing IL-17 to increase. Il-17 can promote osteoclast activity and subsequently escalate bone resorption. The overall mechanism involved in the induction of CCL20 by IL-1β is still unknown and it is the aim of our study to further investigate this signaling pathway.
Previous studies had shown that IL-1βinduce CCL20 in Human gingival fibroblast (HGF) via a NF-κB dependent pathway. We discovered the NOX4 inhibitor, Plumbagin and ROS inhibitor, NAC can inhibit the above mentioned pathway. And IL-1β can induce NOX4 and ROS in HGF as well. This proved that the signaling pathway of CCL20 induction by IL-1βis NOX4 dependent. Furthermore, we also discovered that Curcumin has the ability to inhibit IL-1β from inducing NOX4 and CCL20 in HGF. This finding may be useful in developing future adjunctive therapy in treating periodontal disease. |
URI: | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/50907 |
DOI: | 10.6342/NTU201600684 |
全文授權: | 有償授權 |
顯示於系所單位: | 臨床牙醫學研究所 |
文件中的檔案:
檔案 | 大小 | 格式 | |
---|---|---|---|
ntu-105-1.pdf 目前未授權公開取用 | 968.33 kB | Adobe PDF |
系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。