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