Administration of FR167653, a New Anti-Inflammatory Compound, Inhibits Aspirin-Induced Gastric Mucosal Injury in Rats

Neutrophils activation and inflammatory cytokines play a critical role in aspirin-induced gastric mucosal injury. FR167653 was first discovered to be a potent inhibitor of interleukin (IL)-1β and tumor necrosis factor-α (TNF-α) production. The purpose of this study is to investigate the anti-inflamm...

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Bibliographic Details
Published in:Journal of Clinical Biochemistry and Nutrition 2006, Vol.39(2), pp.69-74
Main Authors: Ichikawa, Hiroshi, Yoshida, Norimasa, Takagi, Tomohisa, Handa, Osamu, Naito, Yuji, Okanoue, Takeshi, Yoshikawa, Toshikazu
Format: Article
Language:English
Subjects:
Aspirin
FR167653
IL-1β
NSAID
TNF-α
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Summary:Neutrophils activation and inflammatory cytokines play a critical role in aspirin-induced gastric mucosal injury. FR167653 was first discovered to be a potent inhibitor of interleukin (IL)-1β and tumor necrosis factor-α (TNF-α) production. The purpose of this study is to investigate the anti-inflammatory effects against aspirin-induced gastric mucosal injury in rats. The intragastric administration of acidified aspirin induced hyperemia and hemorrhagic erosions in rat stomachs. The increase in the total gastric erosive area after aspirin administration was significantly inhibited by treatment with FR167653 in a dose-dependent manner. The increases in thiobarbituric acid-reactive substances, myeloperoxidase activity and the contents of TNF-α and IL-1β in gastric mucosa after aspirin administration were both significantly inhibited by pre-treatment with FR167653. Based on these data, the beneficial effects of FR167653 on aspirin-induced gastric mucosal injury may be attributed to its anti-inflammatory properties.
ISSN:0912-0009
1880-5086
DOI:10.3164/jcbn.39.69