Hui-xiang Yang1, Yan-rong Yi. 1. Department of Gastroenterology, Xiangya Hospital, Central South University, Changsha 410008, China. yang_hx430@163.com
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.
OBJECTIVE: To explore the curative effect and the mechanism of interferon-alpha (IFN-alpha) on ratliver 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. Ratliver 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.