Inflammation Research

, Volume 57, Issue 2, pp 84–91

Dextran sulfate sodium-induced acute colonic inflammation in angiotensin II type 1a receptor deficient mice

Authors

  • K. Katada
    • Inflammation and ImmunologyKyoto Prefectural University of Medicine
    • Centre for Critical Illness ResearchLawson Health Research Institute
    • Molecular Gastroenterology and Hepatology, Graduate School of Medical ScienceKyoto Prefectural University of Medicine
  • T. Suzuki
    • Inflammation and ImmunologyKyoto Prefectural University of Medicine
  • T. Okuda
    • Inflammation and ImmunologyKyoto Prefectural University of Medicine
  • K. Mizushima
    • Inflammation and ImmunologyKyoto Prefectural University of Medicine
  • T. Takagi
    • Biomedical Safety ScienceKyoto Prefectural University of Medicine
  • H. Ichikawa
    • Inflammation and ImmunologyKyoto Prefectural University of Medicine
  • Y. Naito
    • Medical Proteomics, Graduate School of Medical ScienceKyoto Prefectural University of Medicine
  • G. Cepinskas
    • Centre for Critical Illness ResearchLawson Health Research Institute
  • T. Yoshikawa
    • Inflammation and ImmunologyKyoto Prefectural University of Medicine
    • Biomedical Safety ScienceKyoto Prefectural University of Medicine
    • Medical Proteomics, Graduate School of Medical ScienceKyoto Prefectural University of Medicine
Article

DOI: 10.1007/s00011-007-7098-y

Cite this article as:
Katada, K., Yoshida, N., Suzuki, T. et al. Inflamm. res. (2008) 57: 84. doi:10.1007/s00011-007-7098-y

Abstract.

Objective:

Angiotensin II (Ang II) receptor blockers have been reported to contribute to cytoprotective effects in various organs. However, the role of renin-angiotensin system (RAS) in modulation of the inflammatory bowel disease (IBD) remains unclear. In this study we assessed the role of angiotensin II type 1a (AT1a) receptor on the outcome of dextran sulfate sodium (DSS)-induced acute colitis by employing AT1a receptor deficient mice.

Materials and methods:

The acute colitis was induced in wild type (WT) and AT1a receptor deficient mice by giving orally 3% DSS in drinking water for 7 days.

Results:

Induction of DSS colitis resulted in up-regulation of Ang II and AT1a receptor in the colonic mucosa of WT mice. In parallel, loss of body weight, an increase in disease activity index (DAI), and the shortening of colon were found in DSS-challenged WT mice. In addition, an increase in thiobarbituric acid (TBA)-reactive substances and myeloperoxidase (MPO) activity, along with the up-regulation of tumor necrosis factor (TNF)-α were detected in the colonic mucosa of DSS-challenged WT mice. The endpoints mentioned above were significantly ameliorated in DSS-challenged AT1a receptor deficient mice.

Conclusions:

RAS is involved in the pathophysiology of DSS-induced colitis and AT1a receptor may be a novel therapeutic target for the treatment of IBD.

Keywords:

Experimental colitisAT1a receptorAngiotensin IIInflammationTNF-α
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Copyright information

© Birkhaueser 2008