title: Potential protective effect of honey against paracetamol-induced hepatotoxicity.
abstract: BACKGROUND
  Paracetamol overdose causes severe hepatotoxicity that leads to liver failure in both humans and experimental animals. The present study investigates the protective effect of honey against paracetamol-induced hepatotoxicity in Wistar albino rats. We have used silymarin as a standard reference hepatoprotective drug.
  
  
  METHODS
  Hepatoprotective activity was assessed by measuring biochemical parameters such as the liver function enzymes, serum alanine aminotransferase (ALT) and serum aspartate aminotransferase (AST). Equally, comparative effects of honey on oxidative stress biomarkers such as malondialdyhyde (MDA), reduced glutathione (GSH) and glutathione peroxidase (GPx) were also evaluated in the rat liver homogenates.  We estimated the effect of honey on serum levels and hepatic content of interleukin-1beta (IL-1β) because the initial event in paracetamol-induced hepatotoxicity has been shown to be a toxic-metabolic injury that leads to hepatocyte death, activation of the innate immune response and upregulation of inflammatory cytokines.
  
  
  RESULTS
  Paracetamol caused marked liver damage as noted by significant increased activities of serum AST and ALT as well as the level of Il-1β. Paracetamol also resulted in a significant decrease in liver GSH content and GPx activity which paralleled an increase in Il-1β and MDA levels. Pretreatment with honey and silymarin prior to the administration of paracetamol significantly prevented the increase in the serum levels of hepatic enzyme markers, and reduced both oxidative stress and inflammatory cytokines. Histopathological evaluation of the livers also revealed that honey reduced the incidence of paracetamol-induced liver lesions.
  
  
  CONCLUSIONS
  Honey can be used as an effective hepatoprotective agent against paracetamol-induced liver damage.
authors.affiliation: Department of Pharmacology and Toxicology, Cairo University, Cairo, Egypt. Remogalal@yahoo.com
authors.forename: Reem M
authors.initials: RM
authors.lastname: Galal
authors.forename: Hala F
authors.initials: HF
authors.lastname: Zaki
authors.forename: Mona M
authors.initials: MM
authors.lastname: Seif El-Nasr
authors.forename: Azza M
authors.initials: AM
authors.lastname: Agha
mesh_terms: D000082:Acetaminophen / Q000633:toxicity*; D000410:Alanine Transaminase / Q000097:blood; D018712:Analgesics, Non-Narcotic / Q000633:toxicity*; D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D001219:Aspartate Aminotransferases / Q000097:blood; D056486:Chemical and Drug Induced Liver Injury / Q000097:blood / Q000473:pathology / Q000517:prevention & control*; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006722:Honey; D053583:Interleukin-1beta / Q000097:blood / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D012838:Silymarin / Q000627:therapeutic use
chemical_list: D018712:Analgesics, Non-Narcotic; D000975:Antioxidants; D053583:Interleukin-1beta; D012838:Silymarin; D000082:Acetaminophen; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005978:Glutathione