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Updated: Feb 12, 2026

Murine Distal Colostomy, A Novel Model of Diversion Colitis in C57BL/6 Mice
Published on: July 12, 2018
Cardiotrophin-1 attenuates experimental colitis in mice.
Vanessa Prieto-Vicente1,2, Ana I Sánchez-Garrido1,2, Víctor Blanco-Gozalo3
1Department of Gastroenterology, University Hospital of Salamanca, Salamanca 37007, Spain.
Endogenous cardiotrophin-1 (CT-1) protects against ulcerative colitis. Supplementing with CT-1 reduces colon damage and inflammation, suggesting it as a potential therapy for ulcerative colitis.
Area of Science:
- Gastroenterology
- Immunology
- Molecular Biology
Background:
- Cardiotrophin-1 (CT-1) exhibits protective effects in various organs.
- The role of CT-1 in ulcerative colitis (UC) pathogenesis and treatment remains to be fully elucidated.
Purpose of the Study:
- To investigate the role of endogenous CT-1 in experimental UC.
- To evaluate the therapeutic potential of exogenous CT-1 in ameliorating UC symptoms.
Main Methods:
- Ulcerative colitis was induced in CT-1 knockout and wild-type mice using dextran sulphate sodium (DSS).
- Exogenous CT-1 or vehicle was administered to colitic mice, and disease activity, inflammatory markers, colon damage, apoptosis, and bacterial translocation were assessed.
Main Results:
- CT-1 knockout mice exhibited exacerbated colon damage and disease severity compared to wild-type mice.
- Exogenous CT-1 treatment significantly reduced colon damage, disease activity index, and key inflammatory markers (TNF-α, INFγ, IL-17, iNOS).
- CT-1 treatment also decreased apoptosis, enhanced NFκB and STAT3 activation, and prevented bacterial translocation.
Conclusions:
- Endogenous CT-1 plays a crucial role in the colon's defense and repair mechanisms against ulcerative lesions.
- Exogenous CT-1 demonstrates significant therapeutic potential for ulcerative colitis by exerting anti-inflammatory and anti-apoptotic effects.
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