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Murine Colitis Modeling using Dextran Sulfate Sodium (DSS)
Published on: January 19, 2010
Colonic antioxidant status in dextran sulfate-induced colitis in mice
A C Blackburn1, W F Doe, G D Buffinton
1Division of Molecular Medicine, John Curtin School of Medical Research, Australian National University; and *Inflammatory Bowel Disease Research Unit, The Canberra Hospital, Canberra, A.C.T., Australia.
Inflammatory Bowel Diseases
|January 4, 2013
Summary
Inflammatory bowel disease (IBD) involves oxidative stress. Dextran sulfate-induced colitis in mice showed decreased antioxidants and increased injury markers, mirroring human IBD, supporting this model for therapeutic development.
Area of Science:
- Biochemistry
- Gastroenterology
- Immunology
Background:
- Reactive oxygen and nitrogen species contribute to mucosal damage in inflammatory bowel disease (IBD).
- Understanding oxidative stress markers in IBD models is crucial for therapeutic development.
Purpose of the Study:
- Investigate endogenous antioxidants and oxidative injury markers in dextran sulfate-induced colitis in mice.
- Evaluate the relevance of this mouse model to human IBD pathogenesis.
Main Methods:
- Induce colitis in mice using 5% dextran sulfate in drinking water for 8 days.
- Analyze colonic mucosa for radical scavenging capacity, antioxidant levels (lipophilic and aqueous), and thiol markers.
- Measure myeloperoxidase activity to assess neutrophil infiltration.
Main Results:
- Dextran sulfate induced significant neutrophil infiltration (3.3-fold increase in myeloperoxidase activity).
- Reduced levels of total radical scavenging capacity, ubiquinol-9, and ascorbate were observed.
- Increased levels of α-tocopherol and urate were noted, alongside decreased glyceraldehyde-3-phosphate dehydrogenase activity and reduced thiol content.
Conclusions:
- Dextran sulfate-induced colitis in mice exhibits oxidative stress patterns similar to human IBD.
- This model is relevant for studying oxidative mucosal injury in IBD.
- The model supports research into novel therapeutic strategies for IBD.
