Curative effect of interferon-alpha on rat liver fibrosis induced by CCl4.
- Author:
Hui-xiang YANG
1
;
Yan-rong YI
Author Information
1. Department of Gastroenterology, Xiangya Hospital, Central South University, Changsha 410008, China. yang_hx430@163.com
- Publication Type:Journal Article
- MeSH:
Actins;
biosynthesis;
genetics;
Animals;
Carbon Tetrachloride;
Carbon Tetrachloride Poisoning;
Collagen Type I;
biosynthesis;
genetics;
Interferon-alpha;
therapeutic use;
Liver Cirrhosis, Experimental;
chemically induced;
drug therapy;
metabolism;
Male;
RNA, Messenger;
biosynthesis;
genetics;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Transforming Growth Factor beta1;
biosynthesis;
genetics
- From:
Journal of Central South University(Medical Sciences)
2008;33(10):919-925
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the curative effect and the mechanism of interferon-alpha (IFN-alpha) on rat liver fibrosis induced by CCl4.
METHODS:Thirty-nine male SD rats were randomly divided into 3 groups. The rats in the normal control group (n=10) received subcutaneous injection of peanut oil (0.003 mL/g body weight) for 10 weeks. Rat liver fibrosis was induced in 29 rats by 0.003 mL/g subcutaneous injection of 40% CCl4 (CCl4: peanut oil = 2:3), twice weekly for 10 weeks. In the 7th week, these 29 rats were randomly divided into a liver fibrosis group without treatment (n=15) and an IFN-alpha treatment group (n=14), which received subcutaneous injection of IFN-alpha-2b at 10(6) units per rat. The rats' liver tissue was collected and HE and Masson staining were performed to observe of pathological changes, stage of liver fibrosis,and semi-quantitative scoring. Immunohistochemistry was used to detect the expression of Collagen I, alpha-smooth muscle actin (alpha-SMA),and transforming growth factor-beta1 (TGF-beta1) in the rat liver.
RESULTS:The stage of liver fibrosis, semi-quantitative scoring of Masson staining, and immunohistochemical staining of Collagen I in the liver fibrosis group were significantly higher than those of the normal controls (All P<0.01), and those in the IFN-alpha treatment group were significantly lower than those of the liver fibrosis group(P<0.05). The semi-quantitative immunohistochemical scoring of alpha-SMA and TGF-beta1 in the liver fibrosis group was significantly higher than those of the normal control (All P<0.01), and that in the IFN-alpha treatment group was significantly lower than that of the liver fibrosis group (All P<0.05).
CONCLUSION:Treatment of IFN-alpha can decrease the liver fibrogenesis induced by CCl4 in rats. The anti-fibrosis effect of IFN-alpha may be attributed to the inhibition of the hepatic stellate cells' activation to decrease TGF-beta1 expression.
