The changes of advanced glycation end products in a rat liver fibrosis model and the interventional effect of aminoguanidin.
- Author:
Fu-sheng GAO
1
;
Bin LIU
;
Yu-tao ZHAN
;
Xiao-lin SHI
;
Jing-xiu ZHANG
;
Ning WANG
;
Yan DING
;
Xin-ji XIE
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Glycation End Products, Advanced; metabolism; Guanidines; therapeutic use; Liver; metabolism; pathology; Liver Cirrhosis, Experimental; chemically induced; drug therapy; metabolism; Male; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Hepatology 2006;14(3):178-182
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the changes of advanced glycation end products (AGEs) in different phases of a rat liver fibrosis model induced by CCl4, and the interventional effect of aminoguanidin (AG).
METHODSFifty-four SD rats were divided into three groups: a control group, a CCl4 model group and an intervention group. Their blood serum AGEs and hyaluronic acid (HA) and AGEs in their liver homogenates were measured. These measurements were correlatively assessed to the degrees of liver fibrosis at different phases of the rat model before and after the intervention with aminoguanidin.
RESULTSThe content of AGEs in their blood sera and liver homogenates, and the level of blood serum HA, and the score of liver fibrosis degree at week 12 in our rat liver fibrosis mode groups were significantly higher than those in the control group (P < 0.01). In the intervention group with aminoguanidin, these figures were lower than those in the liver fibrosis model group (P < 0.05). The content of AGEs in their blood sera and liver homogenates had a linear correlation with the level of HA in their blood sera.
CONCLUSIONThe contents of AGEs in their blood sera and liver homogenates were increased in the late phase of our rat liver fibrosis model. To some extent, the level of AGEs may reflect the fibrosis degree of the rat livers. Aminoguanidin has an interventional effect in our CCl4 induced rat liver fibrosis model.