Rebamipide reduces indomethacin-induced gastric injury in mice via down-regulation of ICAM-1 expression

被引:17
作者
Hiratsuka, T [1 ]
Futagami, S [1 ]
Shindo, T [1 ]
Hamamoto, T [1 ]
Ueki, N [1 ]
Suzuki, K [1 ]
Shinji, Y [1 ]
Kusunoki, M [1 ]
Shinoki, K [1 ]
Wada, K [1 ]
Miyake, K [1 ]
Gudis, K [1 ]
Tsukui, T [1 ]
Sakamoto, C [1 ]
机构
[1] Nippon Med Coll, Dept Internal Med 3, Bunkyo Ku, Tokyo 1138603, Japan
关键词
intercellular adhesion molecule-1; rebamipide; indomethacin; neutrophil;
D O I
10.1007/s10620-005-2811-6
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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. Pretreatment 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.
引用
收藏
页码:S84 / S89
页数:6
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