Trinitrobenzene sulfonic acid(TNBS)에 의해 유도된 대장 손상에서 TNF-α, IL-1β 및 ICAM-1의 발현 조절을 통한 rebamipide의 방어효과

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Title
Trinitrobenzene sulfonic acid(TNBS)에 의해 유도된 대장 손상에서 TNF-α, IL-1β 및 ICAM-1의 발현 조절을 통한 rebamipide의 방어효과
Author(s)
Y H Kim; S J Kim; H G Hwang; S C Choi; Y R Kim; K S Kim; C Kim; D H Choi; J T Oh; G D Kim; H W Kim; C D Jun; Chun Jeih Ryu; Y T Chung; M K Choi; J M Oh
Bibliographic Citation
Korean Journal of Anatomy, vol. 37, no. 2, pp. 149-155
Publication Year
2004
Abstract
During inflammation of the colon, cells of the gut mucosa produce or express numerous inflammatory mediators, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and intercellular adhesion molecule 1 (ICAM-1). These mediators have been implicated as contributory factors to the inflammatory process, which results in colitis during inflammatory bowel disease (IBD). Rebamipide is an anti-gastric ulcer drug with anti-inflammatory properties in vivo and in vitro. The effects of Rebamipide on IBD have not been largely evaluated. Therefore, this study investigated the potential of Rebamipide to regulate the production of inflammatory mediators such as TNF-α, IL-1β, and ICAM-1. Mice with trinitrobenzene sulfonic acid (TNBS)-induced colitis (IBD animal model), were treated intrarectally with 2 mM Rebamipide. Body weight, macro- and micro-histological scores, and activity were evaluated. As an index of tissue edema, the thickness of the colonic wall was measured between the serosal surface and the luminal surface of the mucosa. TNF-α, IL-1β, and ICAM-1 were detected by immunohistochemical staining. Rebamipide treatment of mice exhibiting TNBS-induced colitis dramatically improved the clinical and histopathological findings of inflammation. In addition, Rebamipide suppressed TNF-α, IL-1β, and ICAM-1 expression in TNBS-treated animals. Taken together, these findings suggest that Rebamipide is a potential therapeutic agent for treating patients with IBD.
Keyword
rebamipideIBMTNBSTNF-αIL-1βICAM-1
ISSN
1225-1305
Publisher
Korea Soc-Assoc-Inst
Type
Article
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1. Journal Articles > Journal Articles
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