title: Abnormal expressions of hepatocellular proteins and extracellular matrix in CCL4-induced liver injury in rats.
abstract: OBJECTIVE
  To evaluate the effects of carbon tetrachloride (CCl4) on the expressions of both intracellular proteins and extracellular matrix and the protective role of taurine.
  
  
  METHODS
  Forty Sprague-Dawley rats were divided into five groups: 1.5% taurine, CCl4, CCl4 + 0.5% taurine, CCl4 + 1.5% taurine and control. CCl4 was given ig at a dose of 500 mg/kg body weight, twice a week for 5 weeks. The taurine solution or tap water was given to the rats for drinking. The sections (4 microns) of rat liver were stained with haematoxylin and eosin, immunohistochemistry or colloid silver methods.
  
  
  RESULTS
  The animals treated with 1.5% taurine and control had normal liver structures. Light microscopic examination of sections of the liver taken 5 weeks after dosing of CCl4 showed hydropic degeneration of hepatocytes around the central veins and lipid vacuolation in mid-zonal and some periportal hepatocytes. Necrotic cells and neutrophil infiltration around most central veins as well as hepatocytes showing various stages of mitosis indicative of regeneration were observed. These histopathological changes in the animals treated with CCl4 alone showed more extensive and severe lesions than those seen in the animals treated with CCl4 plus taurines. The incidences of PCNA and p53 antigen positive hepatocytes, and the numbers of nuclear apoptotic bodies and AgNORs granules were markedly higher in the CCl4-treated animals than in those protected with taurine. Declined and unevenly distributed expressions of LN and FN were seen in the CCl4 treated rats.
  
  
  CONCLUSIONS
  Both the damage of hepatocellular DNA and the abnormal expressions of hepatic extracellular matrix were observed in the CCl4-treated rats. Taurine, in this study, not only inhibited hepatocellular degeneration, necrosis and DNA damage, but also inhibited the lesion of extracellular matrix induced by CCl4.
authors.affiliation: School of Public Health, Nanjing Medical University.
authors.forename: J
authors.initials: J
authors.lastname: Zhou
authors.forename: J
authors.initials: J
authors.lastname: Zhou
authors.forename: X
authors.initials: X
authors.lastname: Zhong
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.forename: X
authors.initials: X
authors.lastname: Yang
mesh_terms: D000818:Animals; D017209:Apoptosis; D002251:Carbon Tetrachloride / Q000633:toxicity; D056486:Chemical and Drug Induced Liver Injury; D005109:Extracellular Matrix / Q000378:metabolism; D005260:Female; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008107:Liver Diseases / Q000378:metabolism*; D008297:Male; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013654:Taurine / Q000494:pharmacology; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D018809:Proliferating Cell Nuclear Antigen; D016159:Tumor Suppressor Protein p53; D013654:Taurine; D002251:Carbon Tetrachloride