title: [Expression of Fas antigen and Fas ligand in acute liver injury induced by carbon tetrachloride in rat].
abstract: OBJECTIVE
  To investigate the dynamics of expression of Fas antigen and Fas ligand (FasL) in a rat model of carbon tetrachloride-induced acute liver injury, and explore the role of apoptosis in liver injury.
  
  
  METHODS
  Thirty-five healthy male Wistar rats were randomly divided into normal control group and experiment group, and the latter group was divided into six subgroups: 3, 9, 16, 24, 36 and 48 hours groups with 5 rats in each group. The liver injury was induced by carbon tetrachloride. Sections of liver tissue were stained with hematoxylin and eosin and observed under optical microscope. Fas antigen and FasL in rat liver were determined at different time points with immunohistochemical method. Hepatocytes apoptosis were observed with terminal deoxynucleotidyl-transferase mediated dUTP-biotin nick end labeling (TUNEL) method. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentration in the liver tissues were analyzed at the same time point. Serum aspartate aminotransferase (ALT) and alanine aminotransferase (AST) levels were also determined.
  
  
  RESULTS
  Fas antigen and FasL were expressed in the liver tissues of control rats. Following carbon tetrachloride challenge, severe liver injury took place in rats as revealed under microscope and a large amount of hepatocytes apoptosis was found. Hepatic Fas and FasL expression were both increased markedly from 3 to 48 hours after carbon tetrachloride challenge in experiment group. Liver MDA concentration and serum ALT and AST were elevated significantly, while SOD activity decreased remarkably in the experiment group compared with control group (P<0.05 or P<0.01).
  
  
  CONCLUSIONS
  Expression of Fas/FasL is remarkably induced in acute liver injury and accords with the changes of hepatocytes apoptosis, which suggests that apoptosis mediated by Fas/FasL may play an important role in the pathogenesis of acute liver injury.
authors.affiliation: Institute of Hepatitis, Youan Hospital, Capital University of Medical Sciences, Beijing 100069, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Wen
authors.forename: Feng
authors.initials: F
authors.lastname: Ren
authors.forename: Yan
authors.initials: Y
authors.lastname: Liu
authors.forename: Zhi-ming
authors.initials: ZM
authors.lastname: Wu
authors.forename: Jin-yuan
authors.initials: JY
authors.lastname: Zhao
mesh_terms: D000818:Animals; D017209:Apoptosis; D002251:Carbon Tetrachloride; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D053222:Fas Ligand Protein / Q000378:metabolism*; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008297:Male; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D019014:fas Receptor / Q000378:metabolism*
chemical_list: D053222:Fas Ligand Protein; C491898:Fas protein, rat; C505662:Faslg protein, rat; D019014:fas Receptor; D002251:Carbon Tetrachloride