English  |  正體中文  |  简体中文  |  Items with full text/Total items : 27248/39091
Visitors : 2415687      Online Users : 73
RC Version 4.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Adv. Search
LoginUploadHelpAboutAdminister

Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/37359

Title: Apocynin alleviated hepatic oxidative burden and reduced liver injury in hypercholesterolaemia
Authors: Long-Sheng Lu;Chau-Chung Wu;Li-Man Hung;Meng-Tsan Chiang;Ching-Ting Lin;Chii-Wann Lin
Contributors: 國立臺灣海洋大學:食品科學系
Keywords: apocynin;cholesterol;gp91phox;liver injury;NADPH oxidase
Date: 2007-05
Issue Date: 2016-01-21T06:16:13Z
Publisher: official journal of the International Association for the Study of the Liver
Abstract: Abstract:This study addressed the effects of apocynin, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, on hepatic oxidative burden and liver injury during diet-induced hypercholesterolaemia.
Male Wistar rats were fed a 4% cholesterol-enriched diet for 3 weeks. Apocynin was administered in drinking water concurrently. The high-cholesterol diet (HC) significantly increased the serum level of cholesterol and hepatic cholesterol ester deposition, and these parameters were similar between the HC and high-cholesterol diet plus apocynin (HCA) groups. The HC group showed abnormal liver function tests [alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (Alk-P)] as well as increased Evans blue extravasation and macrophages infiltration. Apocynin treatment could suppress these inflammation-related parameters. In vivo measurement of NADPH-derived cellular autofluorescence suggested that HC increased oxidative stress in hepatocytes. Biochemical analysis of redox status including thiobarbituric acid reactive substances, reduced glutathione, and oxidized glutathione also confirmed the phenomenon. Apocynin treatment was able to alleviate these indices of oxidative burden owing to HC. Furthermore, apocynin-abrogated HC induced gp91(phox) expression, suggesting the involvement of NADPH oxidase in the pathogenesis.
We concluded that apocynin suppressed NADPH oxidase activation and subsequent liver injuries owing to high-cholesterol intake in rats. The impacts of cholesterol metabolism disorders on pathogenesis and progression of steatohepatitis warrant further clinical investigation.
Relation: 27(4),pp.529-537
URI: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/37359
Appears in Collections:[食品科學系] 期刊論文

Files in This Item:

File Description SizeFormat
index.html0KbHTML80View/Open


All items in NTOUR are protected by copyright, with all rights reserved.

 


著作權政策宣告: 本網站之內容為國立臺灣海洋大學所收錄之機構典藏,無償提供學術研究與公眾教育等公益性使用,請合理使用本網站之內容,以尊重著作權人之權益。
網站維護: 海大圖資處 圖書系統組
DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback