期刊
FOOD AND CHEMICAL TOXICOLOGY
卷 50, 期 6, 页码 1992-2001出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2012.03.044
关键词
Gypsophila elegans; Isoorientin-2-O-alpha-L-arabinopyranosyl; Alcohol; Liver fibrosis
资金
- Guangxi Key Laboratory for Prevention & Treatment of Regional HighIncidence Diseases [KFJJ2010-71, KFJJ2011-37, KFJJ2010-22, 0842009-Z11, 0842009-K4]
- Department of Education of Guangxi Province [200911MS28]
- Guangxi Scientific Research & Technology Development [0015048, 101240086, 0322024-5E]
- Guangxi Natural Science Foundation [0731066]
Alcohol abuse is one of the major causes of liver fibrosis, which shows a sharply increasing trend worldwide, yet effective therapeutic options for advanced alcohol fibrosis are limited. Recently we investigated the effect of anti-fibrosis by isoorientin-2-O-alpha-L-arabinopyranosyl (IOA) isolated from Gypsophila elegans. During the experiment, the model group received alcohol only, and treatment groups received the corresponding drugs plus alcohol respectively, while the normal control group received an equal volume of saline. Analysis at the end of 24-week experiments showed that IOA could significantly improve the liver function, as indicated by decreasing levels of alanine transaminase, aspartate transaminase, alkaline phosphatase, gamma-glutamyltransferase, interleukin-6 and tumor necrosis factor-alpha. Moreover, IOA could effectively inhibit collagen deposition and reduce the pathological tissue damage. Research on mechanism showed that IOA was able to markedly reduce lipid peroxidation, recruit the anti-oxidative defense system, and induce HSC apoptosis by down-regulating bcl-2 mRNA, as well as inhibit the expression of alpha-smooth muscle actin and transforming growth factor beta 1 proteins. In short, our results showed that IOA is effective in attenuating hepatic injury and fibrosis in the alcohol-induced rat model, which should be developed as a new drug to treat liver fibrosis and even cirrhosis. (C) 2012 Elsevier Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据