Abstract | BACKGROUND/AIM: Helicobacter pylori (H. pylori) induces cyclooxygenase-2 (COX-2) expression. The aim of this study was to assess the roles of COX-2 and PGE2 receptors (EPs) in gastric defense in H. pylori-infected mice. METHODS: Gastric lesions were induced by oral administration of 0.15N HCl in 60% ethanol (HCl/EtOH) to mice infected with H. pylori, and macroscopically evaluated 30 min later. Mice were administered NS-398 (COX-2 selective inhibitor) concomitantly with selective EP agonists 4 hours before HCl/EtOH challenge. RESULTS: H. pylori infection prevented the gastric damage induced by HCl/ EtOH, and this protective effect was abolished by NS-398. Selective agonists of EP1, EP2, and EP4, but not the EP3 agonist, reversed the inhibitory effect of NS-398 on prevention of damage by H. pylori infection. The EP4 agonist and EP2/EP4 agonists inhibited the increase in TNF-alpha mRNA expression and neutrophilic infiltration caused by NS-398, respectively. CONCLUSION: COX-2-derived PGE2 may play an important role in resistance to HCl/EtOH damage in H. pylori-infected mice by activating EP1, EP2, and EP4.
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Authors | K Taira, T Watanabe, T Tanigawa, M Shiba, K Tominaga, Y Fujiwara, N Oshitani, K Higuchi, T Arakawa |
Journal | Inflammopharmacology
(Inflammopharmacology)
Vol. 15
Issue 3
Pg. 132-8
(Jun 2007)
ISSN: 0925-4692 [Print] Switzerland |
PMID | 19847955
(Publication Type: Journal Article)
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Chemical References |
- Nitrobenzenes
- Ptger1 protein, mouse
- Ptger2 protein, mouse
- Ptger4 protein, mouse
- Receptors, Prostaglandin E
- Receptors, Prostaglandin E, EP1 Subtype
- Receptors, Prostaglandin E, EP2 Subtype
- Receptors, Prostaglandin E, EP4 Subtype
- Sulfonamides
- Tumor Necrosis Factor-alpha
- N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide
- Ethanol
- Ptgs2 protein, mouse
- Cyclooxygenase 1
- Cyclooxygenase 2
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Topics |
- Animals
- Cyclooxygenase 1
(analysis)
- Cyclooxygenase 2
(analysis, physiology)
- Ethanol
(toxicity)
- Female
- Gastric Mucosa
(immunology, microbiology)
- Helicobacter Infections
(immunology)
- Helicobacter pylori
- Mice
- Mice, Inbred C57BL
- Nitrobenzenes
(pharmacology)
- Receptors, Prostaglandin E
(physiology)
- Receptors, Prostaglandin E, EP1 Subtype
- Receptors, Prostaglandin E, EP2 Subtype
- Receptors, Prostaglandin E, EP4 Subtype
- Sulfonamides
(pharmacology)
- Tumor Necrosis Factor-alpha
(physiology)
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