Inhibitory effect of etodolac, a selective cyclooxygenase-2 inhibitor, on stomach carcinogenesis in Helicobacter pylori-infected Mongolian gerbils

The effect of the selective COX-2 inhibitor, etodolac, on Helicobacter pylori ( Hp)-associated stomach carcinogenesis was investigated in Mongolian gerbils (MGs). Hp-infected MGs were fed for 23 weeks with drinking water containing 10 ppm N-methyl- N-nitrosourea. They were then switched to distilled...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2005-08, Vol.334 (2), p.606-612
Main Authors: Magari, Hirohito, Shimizu, Yasuhito, Inada, Ken-ichi, Enomoto, Shotaro, Tomeki, Tatsuji, Yanaoka, Kimihiko, Tamai, Hideyuki, Arii, Kenji, Nakata, Hiroya, Oka, Masashi, Utsunomiya, Hirotoshi, Tsutsumi, Yutaka, Tsukamoto, Tetsuya, Tatematsu, Masae, Ichinose, Masao
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Animals
CARBON MONOXIDE
CARCINOGENESIS
CELL PROLIFERATION
Chemoprevention
COX-2
Cyclooxygenase Inhibitors - administration & dosage
DIET
DNA DAMAGES
Dose-Response Relationship, Drug
DRINKING WATER
Etodolac
Etodolac - administration & dosage
Gerbillinae
GERBILS
Helicobacter Infections - complications
Helicobacter Infections - drug therapy
Helicobacter pylori
Helicobacter pylori - drug effects
INFLAMMATION
MAGNESIUM SULFIDES
Male
MOLECULES
Mongolian gerbils
NEOPLASMS
Precancerous Conditions - drug therapy
Precancerous Conditions - microbiology
STOMACH
Stomach cancer
Stomach Neoplasms - etiology
Stomach Neoplasms - microbiology
Stomach Neoplasms - pathology
Stomach Neoplasms - prevention & control
Treatment Outcome
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Summary:The effect of the selective COX-2 inhibitor, etodolac, on Helicobacter pylori ( Hp)-associated stomach carcinogenesis was investigated in Mongolian gerbils (MGs). Hp-infected MGs were fed for 23 weeks with drinking water containing 10 ppm N-methyl- N-nitrosourea. They were then switched to distilled water and placed on a diet containing 5–30 mg/kg/day etodolac for 30 weeks. We found that etodolac dose-dependently inhibited the development of gastric cancer, and no cancer was detected at a dose of 30 mg/kg/day. Etodolac did not affect the extent of inflammatory cell infiltration or oxidative DNA damage, but it significantly inhibited mucosal cell proliferation and dose-dependently repressed the development of intestinal metaplasia in the stomachs of Hp-infected MGs. These results suggest that COX-2 is a key molecule in inflammation-mediated stomach carcinogenesis and that chemoprevention of stomach cancer should be possible by controlling COX-2 expression or activity.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2005.06.132