Protein Information

ID 178
Name interferon (protein family or complex)
Synonyms Interferon

Compound Information

ID 1392
Name carbon tetrachloride
CAS tetrachloromethane

Reference

PubMed Abstract RScore(About this table)
19001734 Yang HX, Yi YR: [Curative effect of interferon-alpha on rat liver fibrosis induced by CCl4]. Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2008 Oct;33(10):919-25.
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.
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