Piroxicam accelerates development of colitis in T-cell receptor α chain-deficient mice

被引：6

作者：

Nishiyori, Atsushi ^{[1
]}

Nagakura, Yasunori ^{[1
]}

Ichikawa, Katsuomi ^{[1
]}

机构：

[1] Pfizer Inc, Nagoya Labs, Discovery Biol Res, Pfizer Global Res & Dev, Aichi, Japan

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 2009年 / 615卷 / 1-3期

关键词：

Inflammatory bowel disease; Colitis; T-cell receptor alpha deficient mouse; Nonsteroidal anti-inflammatory drug; Piroxicam; Corticosteroid; INFLAMMATORY-BOWEL-DISEASE; IL-10-DEFICIENT MICE; DIFFERENTIATION; INTERLEUKIN-17; PATHOGENESIS; BACTERIA; PATHWAY; MODELS; GAMMA;

D O I：

10.1016/j.ejphar.2009.05.002

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

T-cell receptor a chain (TCR alpha)-deficient mice spontaneously develop colitis that resembles human ulcerative colitis; however, the incidence varies among individuals and takes place lately in the life. We have demonstrated that piroxicam induces colitis in non-colitic TCR alpha-deficient mice, but not wild-type mice, within 14 days. The histological features and cytokine profiles were similar to those seen in spontaneous colitis in TCRa-deficient mice. Dexamethasone prevented piroxicam-induced colitis concurrent with the suppression of interleukin (IL)-1 beta, IL-17, tumor necrosis factor a and interferon gamma. This modified model of colitis could be useful for the evaluation of potential therapeutics for ulcerative colitis. (C) 2009 Elsevier B.V. All rights reserved.

引用

页码：241 / 245

页数：5

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