| Literature DB >> 16184426 |
Tetsuro Hiratsuka1, Seiji Futagami, Tomotaka Shindo, Tatsuhiko Hamamoto, Nobue Ueki, Kenji Suzuki, Yoko Shinji, Masanori Kusunoki, Kei Shinoki, Ken Wada, Kazumasa Miyake, Katya Gudis, Taku Tsukui, Choitsu Sakamoto.
Abstract
Non-steroidal anti-inflammatory drugs (NSAIDs) induced gastric mucosal injury occurs through subsequent events following free radical production derived from activated neutrophils. In this study, we hypothesized that rebamipide, a novel anti-ulcer agent, exerts a protective effect on NSAID-induced gastric injury through its antioxidant properties. The protective effect of rebamipide in a mouse model of indomethacin-induced gastric injury and mechanisms for this effect were investigated. Pre-treatment with rebamipide significantly inhibited indomethacin-induced gastric mucosal injury in mice. Gastric thiobarbituric acid reactive substances (TBARS) levels and myeloperoxidase (MPO) activity substantially increased 3 hr after indomethacin administration. These increases were significantly inhibited by pre-treatment with rebamipide. Furthermore, rebamipide pre-treatment notably decreased intercellular adhesion molecule-1 (ICAM-1) expression that was up-regulated in gastric tissue treated with indomethacin. Therefore, rebamipide may reduce indomethacin-induced gastric mucosal injuries through its antioxidant effect, which inhibits the neutrophil activation step following up-regulation of ICAM-1 expression on endothelial cells.Entities:
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Year: 2005 PMID： 16184426 DOI： 10.1007/s10620-005-2811-6
Source DB: PubMed Journal: Dig Dis Sci ISSN： 0163-2116 Impact factor: 3.199