Please use this identifier to cite or link to this item:
Title: Advanced glycation end products augment experimental hepatic fibrosis.
Authors: Goodwin, Michelle;Herath, Chandana B;Jia, Zhiyuan;Leung, Christopher;Coughlan, Melinda T;Forbes, Josephine M;Angus, Peter W
Affiliation: Department of Medicine, The University of Melbourne, Melbourne, Victoria, Australia
Issue Date: 1-Feb-2013
Citation: Journal of Gastroenterology and Hepatology; 28(2): 369-76
Abstract: Advanced glycation end products (AGEs) are nonenzymatic modifications of proteins by reducing sugars. These compounds accumulate in a number of chronic disease states, contributing to tissue injury via several mechanisms, including activation of the receptor for advanced glycation end products (RAGE). We aimed to investigate whether AGEs can exacerbate chronic liver injury and contribute to hepatic fibrosis.We initially studied the effects of chronic hepatic exposure to high levels of AGEs given intraperitoneally as AGE-rat serum albumin. In a separate experiment, we examined the impact of high AGE exposure in rats following bile duct ligation (BDL).In normal rats, chronic AGE-rat serum albumin administration induced significant increases in α-smooth muscle actin gene and protein expression but did not induce fibrosis or biochemical evidence of liver injury. However, in BDL animals, AGE-bovine serum albumin administration significantly increased hepatic fibrosis as evidenced by increased collagen content and α-smooth muscle actin expression, compared with BDL alone. Furthermore, AGEs increased hepatic oxidative stress and receptor for advanced glycation end products gene expression.These findings suggest that AGEs may contribute to the pathogenesis of chronic liver injury and fibrosis.
Internal ID Number: 23173780
DOI: 10.1111/jgh.12042
Type: Journal Article
Subjects: Actins.genetics.metabolism
Biological Markers.metabolism
Common Bile
Glycosylation End Products, Advanced.administration & dosage.toxicity
Injections, Intraperitoneal
Liver.drug effects.metabolism.pathology
Liver Cirrhosis, Experimental.chemically induced.genetics.metabolism.pathology
Oxidative Stress.drug effects
Rats, Sprague-Dawley
Receptors, Immunologic.drug effects.genetics.metabolism
Serum Albumin.administration & dosage.toxicity
Appears in Collections:Journal articles

Files in This Item:
There are no files associated with this item.

Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.