title: Antifibrotic effects of interleukin-10 on experimental hepatic fibrosis.
abstract: OBJECTIVE
  To study the effects of interleukin-10 on hepatic stellate cells and liver tissue in experimental rats hepatic fibrosis.
  
  
  METHODS
  Rat hepatic fibrosis model induced by carbon tetrachloride was established. Liver tissues were harvested from the rats administered CCl4 with or without IL-10 treatment and the animals of the control group. The expression of TGF-beta1, MMP-2 and TIMP-1 in the liver tissues was measured by S-P immunohistochemistry. In addition, another model was established; HSCs in rats in each group were isolated. RT-PCR was employed to analyze TGF-beta1, MMP-2 and TIMP-1 mRNA expression in cells and immunocytochemistry was performed to detect protein expression of alpha-SMA, NF-kappaB, TGF-beta1, MMP-2 and TIMP-1 in HSCs.
  
  
  RESULTS
  Rat hepatic fibrosis was developed successfully. The fibrosis changes were partially reversed by simultaneous administration of IL-10. The positive signals of TGF-beta1, MMP-2 and TIMP-1 were observed more frequently (P<0.05) in the CCl4-treated group compared to those in the IL-10-treated group and the control group. HSCs were successfully isolated. TGF-beta1, MMP-2 and TIMP-1 mRNA in HSCs increased obviously during the course of hepatic fibrosis, and their levels were decreased after the treatment with IL-10 (P<0.05). The immunocytochemistry positive levels for TGF-beta1, MMP-2, TIMP-1, alpha-SMA and NF-kappaB in the fibrogenesis group were increased significantly compared to the normal group (P<0.01). The positive signals decreased significantly (P<0.05) after the treatment with IL-10.
  
  
  CONCLUSIONS
  The expression of TGF-beta1, MMP-2 and TIMP-1 increased in liver or in HSC of hepatic fibrosis rats and decreased after treatment with IL-10. The IL-10 could inhibit the activation of HSCs and make an antifibrogenic process come into effect in this way.
authors.affiliation: Department of Gastroenterology, Union Hospital of Fujian Medical University, Fuzhou 350001, Fujian Province, China.
authors.forename: Li-Juan
authors.initials: LJ
authors.lastname: Zhang
authors.forename: Wei-Da
authors.initials: WD
authors.lastname: Zheng
authors.forename: Yun-Xin
authors.initials: YX
authors.lastname: Chen
authors.forename: Yue-Hong
authors.initials: YH
authors.lastname: Huang
authors.forename: Zhi-Xin
authors.initials: ZX
authors.lastname: Chen
authors.forename: Sheng-Jun
authors.initials: SJ
authors.lastname: Zhang
authors.forename: Mei-Na
authors.initials: MN
authors.lastname: Shi
authors.forename: Xiao-Zhong
authors.initials: XZ
authors.lastname: Wang
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D004586:Electrophoresis; D005342:Fibrinolysis / Q000502:physiology*; D007150:Immunohistochemistry; D016753:Interleukin-10 / Q000502:physiology*; D008099:Liver / Q000166:cytology; D008106:Liver Cirrhosis, Experimental / Q000378:metabolism*; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D016328:NF-kappa B; D019715:Tissue Inhibitor of Metalloproteinase-1; D053773:Transforming Growth Factor beta1; D016753:Interleukin-10; D020778:Matrix Metalloproteinase 2