title: Allicin, the active component of garlic, prevents immune-mediated, concanavalin A-induced hepatic injury in mice.
abstract: OBJECTIVE
  Allicin, the immunologically active component of garlic, has been found to affect oxidative stress and immune response in several experimental systems. In the present study, we examined the ability of allicin to prevent immune-mediated, concanavalin A (Con A)-induced liver damage in mice.
  
  
  METHODS
  Mice were pretreated with allicin for 7 days before their inoculation with Con A (15 mg/kg). The serum levels of liver enzymes and liver histology were examined 24 h after Con A administration. The effect of Con A and allicin on serum levels of tumor necrosis factor-alpha (TNF-alpha) and nuclear factor-kappaB (NF-kappaB) activation in the liver were examined 2 h after Con A administration, in a separate group of rats, and the effect of allicin on Con A-induced expression of inducible nitric oxide synthase (iNOS) was determined by western blot analysis 24 h after Con A injection.
  
  
  RESULTS
  The histopathologic damage in the mouse livers, and the Con A-induced increase of aminotransferases and TNF-alpha were markedly inhibited in the mice pretreated with allicin before Con A injection (P < 0.01). NF-kappaB binding activity to the nucleus, which increased 2 h after Con A administration, was attenuated by allicin. The expression of iNOS protein which was induced following Con A administration was significantly attenuated by allicin. In vitro studies showed that allicin inhibited TNF-alpha-mediated T cell adhesion to extracellular matrix components and to endothelial cells. Allicin also inhibited TNF-alpha-mediated intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression on human vascular endothelial cells.
  
  
  CONCLUSIONS
  This study demonstrates that immune-mediated liver damage in mice can be prevented by allicin, probably because of its immunomodulatory effects on T cells and adhesion molecules and inhibition of NF-kappaB activation.
authors.affiliation: Department of Gastroenterology, The E. Wolfson Medical Center, Holon, Israel. rafib@tasmc.health.gov.il
authors.forename: Rafael
authors.initials: R
authors.lastname: Bruck
authors.forename: Hussein
authors.initials: H
authors.lastname: Aeed
authors.forename: Eli
authors.initials: E
authors.lastname: Brazovsky
authors.forename: Talia
authors.initials: T
authors.lastname: Noor
authors.forename: Rami
authors.initials: R
authors.lastname: Hershkoviz
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002448:Cell Adhesion / Q000187:drug effects / Q000276:immunology; D003208:Concanavalin A / Q000494:pharmacology; D004220:Disulfides; D005109:Extracellular Matrix / Q000378:metabolism; D005737:Garlic; D006505:Hepatitis / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008024:Ligands; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D018384:Oxidative Stress / Q000276:immunology; D013441:Sulfinic Acids / Q000494:pharmacology*; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D000975:Antioxidants; D004220:Disulfides; D008024:Ligands; D016328:NF-kappa B; D013441:Sulfinic Acids; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D003208:Concanavalin A; D018799:Intercellular Adhesion Molecule-1; C006452:allicin; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; D000410:Alanine Transaminase