Korean J Anat.  2004 Apr;37(2):149-155.

Rebamipide Protects Colonic Damage Induced by Trinitrobenzene Sulfonic Acid (TNBS) via Down-Regulation of TNF-alpha IL-1beta and ICAM-1

Affiliations
  • 1Department of Anatomy, Wonkwang Medical Science Institute, Korea. jmoh@wonkwang.ac.kr
  • 2Department of Internal medicine, Wonkwang Medical Science Institute, Korea.
  • 3Department of Anesthesiology, Wonkwang Medical Science Institute, Korea.
  • 4Department of General Surgery, Wonkwang Medical Science Institute, Korea.
  • 5Department of Diagnostic Radiology, Wonkwang Medical Science Institute, Korea.
  • 6Department of Immunology, School of Medicine, Wonkwang University, Iksan, Korea.
  • 7Department of Emergency, School of Medicine, Chosun University, Korea.
  • 8Laboratory of Immunology Korea Research Institute of Bioscience and Biotechnology, Korea.

Abstract

During inflammation of the colon, cells of the gut mucosa produce or express numerous inflammatory mediators, such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1 beta), 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-alpha, IL-1beta, 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-alpha, IL-1 beta, 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-alpha, IL-1 beta, 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

Rebamipide; IBD; TNBS; TNF-alpha; IL-1 beta; ICAM-1

MeSH Terms

Animals
Body Weight
Colitis
Colon*
Down-Regulation*
Edema
Humans
Inflammation
Inflammatory Bowel Diseases
Intercellular Adhesion Molecule-1*
Interleukin-1beta
Mice
Mucous Membrane
Phenobarbital
Tumor Necrosis Factor-alpha*
Ulcer
Intercellular Adhesion Molecule-1
Interleukin-1beta
Phenobarbital
Tumor Necrosis Factor-alpha
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