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Published on: September 12, 2019
Targeting Inflammation and Oxidative Stress to Improve Outcomes in a TNBS Murine Crohn's Colitis Model
Anisha Apte1, James R Bardill2, Jimena Canchis1
1Laboratory for Fetal and Regenerative Biology, Department of Surgery, University of Arizona Tucson College of Medicine, Banner Children's at Diamond Children's Medical Center, Tucson, AZ 85721, USA.
Cerium oxide nanoparticles conjugated to microRNA 146a (CNP-miR146a) reduced inflammation and oxidative stress in a mouse model of Crohn's disease. This novel compound improved clinical outcomes and decreased inflammatory markers in colitis.
Area of Science:
- Biomedical Engineering
- Nanomedicine
- Gastroenterology
Background:
- Crohn's disease pathogenesis involves inflammation and oxidative stress.
- MicroRNA 146a (miR146a) plays a role in regulating inflammatory responses.
- Cerium oxide nanoparticles (CNPs) possess anti-inflammatory and antioxidative properties.
Purpose of the Study:
- To investigate the therapeutic potential of CNP-miR146a in a mouse model of Crohn's disease.
- To evaluate the efficacy of local CNP-miR146a administration in reducing colonic inflammation.
Main Methods:
- Induction of colitis in Balb/c mice using 2,4,6-Trinitrobenzenesulfonic acid (TNBS) enemas.
- Local administration of CNP-miR146a via enema.
- Assessment of clinical disease activity, weight loss, colonic histology, miR146a expression, and inflammatory cytokine (IL-6, TNF) levels.
Main Results:
- CNP-miR146a enema increased colonic miR146a expression.
- Treated mice showed reduced weight loss and improved histological inflammation scores.
- Significant reduction in IL-6 and TNF gene expression and protein concentrations was observed.
Conclusions:
- Local delivery of CNP-miR146a effectively ameliorates acute experimental colitis.
- CNP-miR146a demonstrates potential as a therapeutic agent for Crohn's disease by reducing inflammatory signaling.
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