Inhibitory effect of etodolac, a selective cyclooxygenase-2 inhibitor, on stomach carcinogenesis in Helicobacter pylori-infected Mongolian gerbils
- Second Dept. of Internal Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama-City, Wakayama 641-0012 (Japan)
- First Dept. of Pathology, Fujita Health University School of Medicine, Toyoake, Aichi 470-1192 (Japan)
- Second Dept. of Internal Medicine, Wakayama Medical Univ., 811-1 Kimiidera, Wakayama-City, Wakayama 641-0012 (Japan)
- Dept. of Pathology, Wakayama Medical Univ., 811-1 Kimiidera, Wakayama-City, Wakayama 641-0012 (Japan)
- First Dept. of Pathology, Fujita Health Univ. School of Medicine, Toyoake, Aichi 470-1192 (Japan)
- Lab. of Pathology, Aichi Cancer Center Research Inst., Aichi 464-8681 (Japan)
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.
- OSTI ID:
- 20710935
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 334, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2005.06.132; PII: S0006-291X(05)01367-7; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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