TITLE

Roles of cyclooxygenase 2 and microsomal prostaglandin E synthase 1 in rat acid reflux oesophagitis

AUTHOR(S)
T. Hayakawa; Fujiwara, Y.; Hamaguchi, M.; Sugawa, T.; Okuyama, M.; Sasaki, E.; Watanabe, T.; Tominaga, K.; Oshitani, N.; Oshitani, K.; Higuchi, K.; Arakawa, T.
PUB. DATE
April 2006
SOURCE
Gut;Apr2006, Vol. 55 Issue 4, p450
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background: Although prostaglondin E2 PGE2), 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. Aims: We examined the dynamics of COX-1, COX-2, mPGES-1, mPGES-2, cytosolic PGES (cPGES), and PGE2 synthetic activity in rat acid reflex oesophagitis and the effects of COX-2 inhibitors on the severity of oesophagitis. Methods: Acid reflux aesophagitis was induced by ligating the transitional region between the forestomach and the glandular portion and wrapping the duodenum near the pylorus. Rats were killed an day 3 (acute phase) or day 21 (chronic phase) after induction of aesophagitis. Results: 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 PGE2 synthesis in oesophageal lesions on bath days 3 and 21. Epithelial proliferation was significantly increased in the basal layer an day 21. Inflammatory cells and epithelial cells of the basal layer exhibited reactions far EP4 in oesophagitis. Conclusion: PGE2 derived from COX-2 and mPGES-1 plays a significant role in the pathogenesis of chronic acid reflex oesophagitis, and possibly in basal hyperplasia and persistent inflammatory cell infiltration.
ACCESSION #
20509014

 

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