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Updated: Jul 30, 2026
Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
[WDSUB1 knockdown alleviates dextran sulfate sodium-induced colitis in mice by inhibiting nuclear factor-κB signaling
1Department of Gastroenterology, First Medical Center of Chinese PLA General Hospital, Beijing 100853, China.
Objective:
To explore the effect of WDSUB1 on dextran sulfate sodium (DSS)-induced inflammatory colon injury in mice and the underlying mechanism.
Methods:
Different WDSUB1 siRNA sequences were transfected into mouse fibroblast L929 cells and the optimal sequence was selected by Western blotting. Twelve male C57BL/6 mice were randomized into two groups for injection of siWDSUB1 or siControl via the caudal vein, followed by treatment with 2.5% DSS in drinking water to establish mouse models of DSS- induced colitis (n=6). The expression level of WDSUB1 in the colon tissue of the mice was detected with Western blotting and RT-PCR, the changes in body weight and fecal condition were recorded, and the clinical symptoms of the mice were evaluated. The mRNA expression levels of IL-6, COX-2 and TNF-α and the protein expression of IκBα and P65 in the colon tissues were detected with RT- PCR and Western blotting, respectively.
Results:
The mRNA and protein expressions of WDSUB1 in the colon tissues were significantly lower in colitis mice with WDSUB1 knock-down than in the control mice. Compared with the control mice, the mice receiving siWDSUB1 injection showed obviously milder weight loss, diarrhea and hematochezia with significantly lower mRNA expressions of COX2, IL-6 and TNFα (P < 0.05) and protein expression of IκBα but without obvious changes in P65 expression in the colon tissue.
Conclusion:
WDSUB1 knockdown can alleviate DSS- induced colitis in mice possibly by inhibiting the NF-κB signaling pathway and decreasing the expression of inflammatory factors in the colon tissues.
Insights
WDSUB1 knockdown alleviates inflammatory colon injury in mice with dextran sulfate sodium (DSS)-induced colitis. This suggests WDSUB1 inhibition may be a therapeutic strategy for inflammatory bowel disease.
Area of Science:
- Inflammation and Immunology
- Gastroenterology
- Molecular Biology
Background:
- Inflammatory bowel disease (IBD) poses a significant health challenge.
- Dextran sulfate sodium (DSS)-induced colitis is a common mouse model for IBD research.
- Understanding the molecular mechanisms underlying colitis is crucial for developing new therapies.
Purpose of the Study:
- To investigate the role of WDSUB1 in DSS-induced colitis.
- To explore the potential of WDSUB1 knockdown as a therapeutic strategy for inflammatory colon injury.
Main Methods:
- siRNA-mediated knockdown of WDSUB1 in mouse fibroblast cells and subsequent validation.
- Induction of colitis in C57BL/6 mice using DSS and administration of siWDSUB1 or siControl.
- Assessment of WDSUB1 expression, clinical symptoms, body weight, and fecal parameters.
- Analysis of inflammatory markers (IL-6, COX-2, TNF-α) and NF-κB signaling pathway components (IκBα, P65) via RT-PCR and Western blotting.
Main Results:
- WDSUB1 knockdown significantly reduced the expression of WDSUB1 in the colon tissue of colitis mice.
- Mice with WDSUB1 knockdown exhibited milder symptoms of colitis, including less weight loss, diarrhea, and hematochezia.
- Knockdown of WDSUB1 led to decreased mRNA expression of inflammatory cytokines (COX-2, IL-6, TNF-α) and reduced IκBα protein levels.
Conclusions:
- WDSUB1 knockdown demonstrates a protective effect against DSS-induced colitis in mice.
- The mechanism likely involves the inhibition of the NF-κB signaling pathway.
- Targeting WDSUB1 may represent a novel therapeutic approach for managing inflammatory colon diseases.
