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Updated: Jul 7, 2026
Murine Colitis Modeling using Dextran Sulfate Sodium (DSS)
Published on: January 19, 2010
Dextran sulfate sodium-induced acute colonic inflammation in angiotensin II type 1a receptor deficient mice
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)-alpha 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.
Insights
The renin-angiotensin system (RAS) plays a role in inflammatory bowel disease (IBD). Blocking the angiotensin II type 1a (AT1a) receptor ameliorates dextran sulfate sodium (DSS)-induced colitis in mice.
Area of Science:
- Gastroenterology
- Immunology
- Pharmacology
Background:
- The renin-angiotensin system (RAS) has known cytoprotective effects in various organs.
- The specific role of RAS in inflammatory bowel disease (IBD) pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the role of the angiotensin II type 1a (AT1a) receptor in dextran sulfate sodium (DSS)-induced acute colitis.
- To evaluate the therapeutic potential of targeting the AT1a receptor in IBD.
Main Methods:
- Acute colitis was induced in wild-type (WT) and AT1a receptor-deficient mice using 3% DSS in drinking water for 7 days.
- Disease progression was monitored by assessing body weight loss, disease activity index (DAI), and colon length.
- Colonic inflammation markers, including thiobarbituric acid (TBA)-reactive substances, myeloperoxidase (MPO) activity, and tumor necrosis factor-alpha (TNF-α) levels, were measured.
Main Results:
- DSS-induced colitis led to increased angiotensin II (Ang II) and AT1a receptor expression in WT mice.
- WT mice exhibited significant body weight loss, increased DAI, colon shortening, and elevated inflammatory markers.
- AT1a receptor-deficient mice showed significantly ameliorated symptoms and reduced inflammation compared to WT mice.
Conclusions:
- The renin-angiotensin system (RAS) is implicated in the pathophysiology of DSS-induced colitis.
- The angiotensin II type 1a (AT1a) receptor represents a potential therapeutic target for inflammatory bowel disease (IBD).
