{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,20]],"date-time":"2026-03-20T20:54:33Z","timestamp":1774040073783,"version":"3.50.1"},"reference-count":32,"publisher":"BMJ","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"published-print":{"date-parts":[[2006,4]]},"abstract":"<jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    Although prostaglandin E\n                    <jats:sub>2<\/jats:sub>\n                    (PGE\n                    <jats:sub>2<\/jats:sub>\n                    ), cyclooxygenase 2 (COX-2), and microsomal prostaglandin E synthase 1 (mPGES-1) are known to play a role in various inflammatory events, their roles in the pathogenesis of gastro-oesophageal reflux disease are not known.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Aims:<\/jats:bold>\n                    We examined the dynamics of COX-1, COX-2, mPGES-1, mPGES-2, cytosolic PGES (cPGES), and PGE\n                    <jats:sub>2<\/jats:sub>\n                    synthetic activity in rat acid reflux oesophagitis and the effects of COX-2 inhibitors on the severity of oesophagitis.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods:<\/jats:bold>\n                    Acid reflux oesophagitis was induced by ligating the transitional region between the forestomach and the glandular portion and wrapping the duodenum near the pylorus. Rats were killed on day 3 (acute phase) or day 21 (chronic phase) after induction of oesophagitis.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:<\/jats:bold>\n                    Expression of COX-2 and mPGES-1 was markedly increased in oesophagitis while modest changes in COX-1, cPGES, and mPGES-2 expression were observed. COX-2 and mPGES-1 were colocalised in epithelial cells of the basal layer, as well as inflammatory and mesenchymal cells in the lamina propria and submucosa. COX-2 inhibitors significantly reduced the severity of chronic oesophagitis but did not affect acute oesophageal lesions. COX-2 inhibitors significantly inhibited the increase in PGE\n                    <jats:sub>2<\/jats:sub>\n                    synthesis in oesophageal lesions on both days 3 and 21. Epithelial proliferation was significantly increased in the basal layer on day 21. Inflammatory cells and epithelial cells of the basal layer exhibited reactions for EP4 in oesophagitis.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion:<\/jats:bold>\n                    PGE\n                    <jats:sub>2<\/jats:sub>\n                    derived from COX-2 and mPGES-1 plays a significant role in the pathogenesis of chronic acid reflux oesophagitis, and possibly in basal hyperplasia and persistent inflammatory cell infiltration.\n                  <\/jats:p>","DOI":"10.1136\/gut.2005.081943","type":"journal-article","created":{"date-parts":[[2005,10,6]],"date-time":"2005-10-06T20:33:19Z","timestamp":1128630799000},"page":"450-456","source":"Crossref","is-referenced-by-count":16,"title":["Roles of cyclooxygenase 2 and microsomal prostaglandin E synthase 1 in rat acid reflux oesophagitis"],"prefix":"10.1136","volume":"55","author":[{"given":"T","family":"Hayakawa","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Y","family":"Fujiwara","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Hamaguchi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T","family":"Sugawa","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Okuyama","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E","family":"Sasaki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T","family":"Watanabe","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K","family":"Tominaga","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N","family":"Oshitani","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K","family":"Higuchi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T","family":"Arakawa","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"239","published-online":{"date-parts":[[2005,10,6]]},"reference":[{"key":"2025120619203749000_55.4.450.1","doi-asserted-by":"publisher","DOI":"10.1053\/gast.1997.v112.pm9178669"},{"key":"2025120619203749000_55.4.450.2","doi-asserted-by":"crossref","first-page":"163","DOI":"10.1016\/S0016-5085(70)80004-X","volume":"58","year":"1970","journal-title":"Gastroenterology"},{"key":"2025120619203749000_55.4.450.3","doi-asserted-by":"crossref","first-page":"299","DOI":"10.1002\/bms.1200160157","volume":"16","year":"1988","journal-title":"Biomed Environ Mass Spectrom"},{"key":"2025120619203749000_55.4.450.4","doi-asserted-by":"publisher","DOI":"10.1097\/00004836-199504000-00030"},{"key":"2025120619203749000_55.4.450.5","first-page":"7384","volume":"266","year":"1992","journal-title":"Proc Natl Acad Sci USA"},{"key":"2025120619203749000_55.4.450.6","first-page":"383","volume":"68\u201369","year":"2002","journal-title":"Prostaglandins Other Lipid Mediat"},{"key":"2025120619203749000_55.4.450.7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M003505200"},{"key":"2025120619203749000_55.4.450.8","doi-asserted-by":"crossref","unstructured":"Trebino CE, Stock JL, Gibbons CP, et al. 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