title: Protective Effects of Vitamin E on Methotrexate-Induced Jejunal Mucosal Damage in Rats.
abstract: OBJECTIVE
  To investigate the possible protective effects of Vitamin E (Vit E) on oxidative stress and jejunal damage in the rat intestinal mucosa after methotrexate (MTX)-induced enterotoxicity.
  
  
  METHODS
  Rats were divided into 3 groups: control, MTX, and MTX+ Vit E; each group contained 8 animals. The control group was given physiological serum in addition to sunflower oil for 3 days. The second group was given sunflower oil with intragastric tube daily, followed by MTX injection (20 mg/kg intraperitoneally). To the third group, starting 3 days before injection, Vit E was given dissolved in sunflower oil (600 mg/kg orally) in addition to MTX injection. Four days after MTX injection the anesthetized rats were sacrificed, and the tissue samples obtained from their jejunums were investigated for histological and biochemical analysis.
  
  
  RESULTS
  Vit E treatment significantly decreased the elevated tissue malondialdehyde levels and increased the reduced glutathione peroxidase and superoxide dismutase activities in comparison to the MTX-treated group. MTX treatment caused severe histopathological injury including mucosal erosions, inflammatory cell infiltration, necrosis, hemorrhage, and villous congestion. Vit E treatment significantly attenuated the severity of intestinal injury caused by MTX via inhibiting induced nitric oxide synthase levels and NF-κB p65 activation.
  
  
  CONCLUSIONS
  Because of its reconstructing and antioxidant effects, Vit E pretreatment may have protective effects in the intestinal tissue of MTX-treated rats.
authors.forename: Busra
authors.initials: B
authors.lastname: Burcu
authors.forename: Mehmet
authors.initials: M
authors.lastname: Kanter
authors.forename: Zeynep Nur
authors.initials: ZN
authors.lastname: Orhon
authors.forename: Oguzhan
authors.initials: O
authors.lastname: Yarali
authors.forename: Rukiye
authors.initials: R
authors.lastname: Karabacak
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D015415:Biomarkers / Q000378:metabolism; D019610:Cytoprotection; D004195:Disease Models, Animal; D006471:Gastrointestinal Hemorrhage / Q000139:chemically induced / Q000517:prevention & control; D005979:Glutathione Peroxidase / Q000378:metabolism; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007579:Jejunal Diseases / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D007583:Jejunum / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008727:Methotrexate; D016328:NF-kappa B / Q000378:metabolism; D009336:Necrosis; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D016328:NF-kappa B; D014810:Vitamin E; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D013482:Superoxide Dismutase; D008727:Methotrexate