title: Effects of selective cyclooxygenase-2 inhibitor and non-selective NSAIDs on Helicobacter pylori-induced gastritis in Mongolian gerbils.
abstract: BACKGROUND
  It is still a point of controversy whether Helicobacter pylori-infected patients are more likely to develop mucosal damage while taking NSAIDs. Selective cyclooxygenase (COX-2) inhibitors may be associated with less severe gastric mucosal damage than conventional NSAIDs, but this association is undefined in H. pylori-induced gastritis. The aim of this study was to evaluate the effects of selective COX-2 and nonselective NSAIDs on H. pylori-induced gastritis.
  
  
  METHODS
  After intragastric administration of indomethacin, NS-398 or vehicle alone, once daily for 5 days in H. pylori-infected and uninfected Mongolian gerbils, we evaluated gastric mucosal damage, inflammatory cell infiltration and prostaglandin E2 (PGE2) concentration. We investigated whether H. pylori infection induced the COX-2 expression.
  
  
  RESULTS
  In H. pylori-uninfected groups, the indomethacin-treated group showed the highest mucosal damage score and the lowest PGE2 concentration. There was no difference in mucosal damage scores and PGE2 concentration between NS-398 and vehicle-alone treated group. In H. pylori-infected groups, there was no difference in mucosal damage scores, irrespective of the type of drugs administered. The indomethacin-treated group showed the lowest PGE2 concentration, similar to that of the NS-398 and vehicle-alone treated groups, both without H. pylori infection. Gastric neutrophil and monocyte infiltration scores were higher in H. pylori-infected groups than in uninfected groups. However, there was no difference in these scores according to the type of drugs administered, within H. pylori-infected or uninfected groups. COX-2 protein expression was observed in H. pylori-infected Mongolian gerbils but not in uninfected ones.
  
  
  CONCLUSIONS
  Our animal study showed that H. pylori infection induced COX-2 expression and increased prostaglandin concentration. Administration of NSAIDs decreased the prostaglandin concentration, but did not increase mucosal damage in H. pylori-induced gastritis. Selective COX-2 inhibitors, instead of conventional NSAIDs, had no beneficial effect on preventing mucosal damage in H. pylori-induced gastritis.
authors.affiliation: Division of Gastroenterology, Department of Internal Medicine, The Catholic University of Korea, Seoul, Korea.
authors.forename: Choon Sang
authors.initials: CS
authors.lastname: Bhang
authors.forename: Hak Sung
authors.initials: HS
authors.lastname: Lee
authors.forename: Sung Soo
authors.initials: SS
authors.lastname: Kim
authors.forename: Ho Jin
authors.initials: HJ
authors.lastname: Song
authors.forename: Yong Jick
authors.initials: YJ
authors.lastname: Sung
authors.forename: Jin Il
authors.initials: JI
authors.lastname: Kim
authors.forename: In Sik
authors.initials: IS
authors.lastname: Chung
authors.forename: Hee Sik
authors.initials: HS
authors.lastname: Sun
authors.forename: Doo Ho
authors.initials: DH
authors.lastname: Park
authors.forename: Youn Soo
authors.initials: YS
authors.lastname: Lee
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology / Q000627:therapeutic use*; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D015232:Dinoprostone / Q000378:metabolism*; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000188:drug therapy* / Q000382:microbiology; D005849:Gerbillinae; D016481:Helicobacter Infections / Q000188:drug therapy; D016480:Helicobacter pylori; D007213:Indomethacin / Q000627:therapeutic use*; D007527:Isoenzymes / Q000037:antagonists & inhibitors / Q000378:metabolism; D008297:Male; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone; D007213:Indomethacin