title: [Curative effect of interferon-alpha on rat liver fibrosis induced by CCl4].
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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Gastroenterology, Xiangya Hospital, Central South University, Changsha 410008, China. yang_hx430@163.com
authors.forename: Hui-xiang
authors.initials: HX
authors.lastname: Yang
authors.forename: Yan-rong
authors.initials: YR
authors.lastname: Yi
mesh_terms: D000199:Actins / Q000096:biosynthesis / Q000235:genetics; D000818:Animals; D002251:Carbon Tetrachloride; D002252:Carbon Tetrachloride Poisoning; D024042:Collagen Type I / Q000096:biosynthesis / Q000235:genetics; D016898:Interferon-alpha / Q000627:therapeutic use*; D008106:Liver Cirrhosis, Experimental / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D053773:Transforming Growth Factor beta1 / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D000199:Actins; D002251:Carbon Tetrachloride; D024042:Collagen Type I; D016898:Interferon-alpha; D012333:RNA, Messenger; D053773:Transforming Growth Factor beta1; C498862:Acta2 protein, rat