title: Intraperitoneal administration of fetuin-A attenuates D-galactosamine/lipopolysaccharide-induced liver failure in mouse.
abstract: BACKGROUND
  Fulminant hepatic failure (FHF) is a devastating syndrome, which sometimes results in death or liver transplantation, in which inflammation would aggravate the development of fetuin-A which would act as an anti-inflammatory factor and may be an available approach to attenuate FHF.
  
  
  OBJECTIVE
  The purpose of this study was to investigate the effects of fetuin-A on D-galactosamine/lipopolysaccharide (D-GalN/LPS)-induced liver failure in mice.
  
  
  METHODS
  A mouse model of FHF induced by D-GalN/LPS was established and fetuin-A was injected intraperitoneally prior to D-GalN/LPS treatment. At different time points after D-GalN/LPS intervention, serum TNF-α and IL-6 levels were measured by ELISA. Fetuin-A mRNA and protein expression in liver tissues was assessed by RT-PCR, Western blotting and immunohistochemical staining. Besides, an observation of liver tissue injury, the apoptosis of hepatocytes, was analyzed by TUNEL assay.
  
  
  RESULTS
  Expression of fetuin-A mRNA and protein in liver tissue were significantly and gradually decreased after D-GalN/LPS administration. A pre-intervention of exogenous fetuin-A significantly improved the liver function, decreased TNF-α and IL-6 expression in peripheral blood, and liver tissue inhibited hepatocyte apoptosis responded to D-GalN/LPS induction so as to decrease the mortality rates of FHF mouse. Meanwhile, fetuin-A was negatively correlated with the hepatic pathological score and TNF-α protein staining in FHF mouse.
  
  
  CONCLUSIONS
  An intraperitoneal injection of fetuin-A attenuates D-GalN/LPS-induced FHF in mice. Fetuin-A might be a protective agent of liver damage partly through inhibiting liver inflammatory response and hepatocyte apoptosis.
authors.affiliation: Department of Infectious Disease, The Third Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
authors.forename: Pan
authors.initials: P
authors.lastname: Zhang
authors.forename: Hong
authors.initials: H
authors.lastname: Shen
authors.forename: Jinlin
authors.initials: J
authors.lastname: Huang
authors.forename: Haichao
authors.initials: H
authors.lastname: Wang
authors.forename: Baoxin
authors.initials: B
authors.lastname: Zhang
authors.forename: Rongrong
authors.initials: R
authors.lastname: Zhou
authors.forename: Baiyun
authors.initials: B
authors.lastname: Zhong
authors.forename: Xuegong
authors.initials: X
authors.lastname: Fan
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D004195:Disease Models, Animal; D005260:Female; D005688:Galactosamine / Q000008:administration & dosage*; D007274:Injections, Intraperitoneal; D008070:Lipopolysaccharides / Q000008:administration & dosage*; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D017093:Liver Failure / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D008111:Liver Function Tests; D051379:Mice; D008807:Mice, Inbred BALB C; D011897:Random Allocation; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D060749:alpha-2-HS-Glycoprotein / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D060749:alpha-2-HS-Glycoprotein; D005688:Galactosamine