title: Hepatoprotective effect of ghrelin on carbon tetrachloride-induced acute liver injury in rats.
abstract: OBJECTIVE
  Recent studies have revealed that ghrelin may be an antioxidant and antiinflammatory agent. Oxidative stress are considered to play a prominent causative role in the development of various hepatic disorders. We investigated whether ghrelin plays a protective role against carbon tetrachloride (CCl(4))-induced acute liver injury in rats.
  
  
  METHODS
  Forty adult male Sprague-Dawley rats were randomly divided into four equal groups as; control, ghrelin, CCl(4) and ghrelin plus CCl(4). Evaluations were made for lipid peroxidation, enzyme activities and biochemical parameters. Pathological histology was also performed.
  
  
  RESULTS
  CCl(4) treatment increased plasma and liver tissue malondialdehyde (MDA) content and plasma nitric oxide (NO) level, and decreased erythrocyte and liver tissue superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities when compared to control group. At the same time, CCl(4) treatment increased the serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alcaline phosphatase (ALP) activities. By contrast, ghrelin pretreatment reduced plasma and liver MDA content and plasma NO level, and increased erythrocyte and liver tissue SOD, CAT and GPx activities when compared with CCl(4)-treated group. Moreover, both ghrelin alone and ghrelin plus CCl(4) treatment elevated serum glucose level. The CCl(4)-induced histopathological changes were also reduced by the ghrelin pretreatment.
  
  
  CONCLUSIONS
  Our results show that ghrelin can be proposed to protect the liver against CCl(4)-induced oxidative damage in rats, and the hepatoprotective effect may be correlated with its antioxidant and free radical scavenger effects.
authors.affiliation: Department of Physiology, Faculty of Veterinary Medicine, University of Erciyes, Kayseri, Turkey. ecetin@erciyes.edu.tr
authors.forename: Ebru
authors.initials: E
authors.lastname: Cetin
authors.forename: Murat
authors.initials: M
authors.lastname: Kanbur
authors.forename: Nazmi
authors.initials: N
authors.lastname: Cetin
authors.forename: Gökhan
authors.initials: G
authors.lastname: Eraslan
authors.forename: Ayhan
authors.initials: A
authors.lastname: Atasever
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002251:Carbon Tetrachloride / Q000633:toxicity*; D002374:Catalase / Q000097:blood; D056486:Chemical and Drug Induced Liver Injury / Q000473:pathology / Q000517:prevention & control*; D019610:Cytoprotection; D054439:Ghrelin / Q000008:administration & dosage*; D005979:Glutathione Peroxidase / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D009336:Necrosis; D009569:Nitric Oxide / Q000097:blood; D018384:Oxidative Stress / Q000187:drug effects; D020011:Protective Agents / Q000008:administration & dosage*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000097:blood
chemical_list: D001786:Blood Glucose; D054439:Ghrelin; D020011:Protective Agents; D009569:Nitric Oxide; D008315:Malondialdehyde; D002251:Carbon Tetrachloride; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase