Involvement of cyclooxygenase-2 in hyperplastic gastritis induced by Helicobacter pylori infection in C57BL/6 mice

Citation
F. Xiao et al., Involvement of cyclooxygenase-2 in hyperplastic gastritis induced by Helicobacter pylori infection in C57BL/6 mice, ALIM PHARM, 15(6), 2001, pp. 875-886
Citations number
50
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Pharmacology,"da verificare
Journal title
ALIMENTARY PHARMACOLOGY & THERAPEUTICS
ISSN journal
0269-2813 → ACNP
Volume
15
Issue
6
Year of publication
2001
Pages
875 - 886
Database
ISI
SICI code
0269-2813(200106)15:6<875:IOCIHG>2.0.ZU;2-A
Abstract
Background and aims: The hyperplastic changes observed in Helicobacter pylo ri-associated gastritis have been considered to increase the risk of gastri c cancer. The aim of this study was to determine whether cyclooxygenase-2 i s involved in the hyperplastic changes in mice infected with H. pylori. Methods: Seven-week-old, male C57BL/6 mice (n=40) were inoculated with the Sydney strain of H. pylori. Control mice (n=40) were treated with vehicle o nly. Half of the infected and control mice were fed an experimental diet co ntaining etodolac (10 mg/kg/day) from 1 week after inoculation until the en d of the experiment. The thickness of gastric pits, COX-2 mRNA and protein levels, and prostaglandin E-2 (PGE(2)) levels in the gastric mucosa were de termined before and 12, and 24 weeks after inoculation. Results: The thickness of gastric pits, COX-2 mRNA and protein levels, and PGE(2) levels were significantly increased at 24 weeks after inoculation of H. pylori compared with the control groups. Treatment with etodolac result ed in significant decreases in PGE(2) production and in the thickness of ga stric pits in the infected groups at 24 weeks after inoculation. Conclusions: Our findings suggest that COX-2 is involved in the development of hyperplastic gastritis caused by H. pylori infection via the production of PGE(2).