title: Induction of cyclooxygenase 2 in gastric mucosal lesions and its inhibition by the specific antagonist delays healing in mice.
abstract: OBJECTIVE
  The role of two forms of cyclooxygenase (COX-1 and COX-2) in gastric mucosal lesions is not well understood. The regulation of both forms of COX and the effect of COX-2 on the repair process of gastric mucosal lesions in mice were investigated.
  
  
  METHODS
  Gastric mucosal erosions and ulcers were induced experimentally in mice. The level of COX messenger RNA (mRNA) was determined by reverse-transcription polymerase chain reaction. COX proteins were detected by Western blot analysis, and COX activity was determined in the presence or absence of NS-398, a specific COX-2 antagonist. The effects of long-term administration of NS-398 on gastric ulcers were examined.
  
  
  RESULTS
  COX-2 mRNA levels were not detected in control conditions but were high during the acute stages of gastric erosions and ulcers. COX-2 protein was detected 5 days after ulcer induction but not in control mice. Gastric ulceration was not associated with a change in COX-1 mRNA and protein levels. Administration of NS-398 to mice with ulcers at acute stages impaired the healing of ulcers.
  
  
  CONCLUSIONS
  High levels of COX-2 mRNA and protein during the acute stages of gastric mucosal lesions may be involved in the repair process of these lesions in mice.
authors.affiliation: Second Department of Internal Medicine, Kobe University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Mizuno
authors.forename: C
authors.initials: C
authors.lastname: Sakamoto
authors.forename: K
authors.initials: K
authors.lastname: Matsuda
authors.forename: K
authors.initials: K
authors.lastname: Wada
authors.forename: T
authors.initials: T
authors.lastname: Uchida
authors.forename: H
authors.initials: H
authors.lastname: Noguchi
authors.forename: T
authors.initials: T
authors.lastname: Akamatsu
authors.forename: M
authors.initials: M
authors.lastname: Kasuga
mesh_terms: D019342:Acetic Acid; D000143:Acids; D000818:Animals; D015153:Blotting, Western; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004790:Enzyme Induction; D000431:Ethanol; D005753:Gastric Mucosa / Q000378:metabolism* / Q000473:pathology; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism*; D008297:Male; D008565:Membrane Proteins; D051379:Mice; D009578:Nitrobenzenes / Q000494:pharmacology; D016133:Polymerase Chain Reaction; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D012016:Reference Values; D013272:Stomach Diseases / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D013276:Stomach Ulcer / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D013449:Sulfonamides / Q000494:pharmacology; D014158:Transcription, Genetic; D014945:Wound Healing / Q000187:drug effects
chemical_list: D000143:Acids; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D008565:Membrane Proteins; D009578:Nitrobenzenes; D012333:RNA, Messenger; D013449:Sulfonamides; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; D000431:Ethanol; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; C496512:Ptgs1 protein, mouse; D019342:Acetic Acid