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Updated: Jan 1, 2026
Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
Galactooligosaccharides protects against DSS-induced murine colitis through regulating intestinal flora and
Hongqian Chu1, Xi Tao2, Zhaogang Sun3
1Department of Toxicology, School of Public Health, Peking University, Beijing 100191, PR China; Translational Medicine Center, Beijing Chest Hospital, Capital Medical University, Beijing 101149, PR China; Beijing Key Laboratory in Drug Resistant Tuberculosis Research, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing 101149, PR China.
Background/Aims:
Previous studies have demonstrated that Galactooligosaccharides (GOS), known as "bifidus factor", has anti-inflammatory effects. Colitis, a kind of colonic inflammatory damage could be induced by different chemicals. The pathogenesis and mechanism of colitis remains unclear, and may be related to intestinal microflora, genetic susceptibility or immune factors. The aim is to explore the effects of GOS on intestinal flora and its anti-inflammatory effects in Dextran Sulfate Sodium (DSS) induced murine colitis and extrapolate the underlying mechanism.
Main Methods:
Initially, 5% DSS was used to induced colitis by free access to drinking water for 5-7 days. Then the mice were treated with GOS 1 day after DSS treatment. Colon samples were evaluated grossly using a microscope. The percentage of Treg and Th17 cells was analyzed by flow cytometry. The levels of cytokines secretion and mRNA expression were detected by ELISA and real-time PCR. The level of protein was detected by western blot.
Key Findings:
GOS attenuated DSS induced body weight loss and also reduced the increase in disease index caused by DSS. GOS ameliorated DSS induced colonic histological damage. The protective effect of GOS on DSS induced colitis may be partly attributed to intestinal flora regulation and Th17/Treg imbalance. Furthermore, GOS markedly decreased cytokines (IL-6, IL-18, IL-13 and IL-33) secretion and mRNA expression in colon tissues, through inhibiting activation of NF-κB pathways.
Significance:
GOS could prevent the DSS induced colitis through intestinal flora regulation and reduce the secretion of inflammation related cytokines relying on the NF-κB signaling pathway.
Insights
Galactooligosaccharides (GOS) reduce inflammation in colitis by regulating gut microbiota and inhibiting the NF-κB pathway. This study shows GOS protects against Dextran Sulfate Sodium (DSS)-induced colitis in mice.
Area of Science:
- Gastroenterology
- Immunology
- Microbiology
Background:
- Galactooligosaccharides (GOS) exhibit anti-inflammatory properties.
- Colitis pathogenesis involves intestinal microflora, genetics, and immune factors.
- Dextran Sulfate Sodium (DSS) is a common inducer of experimental colitis.
Purpose of the Study:
- To investigate the effects of GOS on intestinal flora in DSS-induced murine colitis.
- To elucidate the anti-inflammatory mechanisms of GOS in colitis.
- To explore the role of GOS in regulating immune responses and gut microbiota.
Main Methods:
- Colitis induced in mice using 5% DSS.
- Mice treated with GOS post-DSS induction.
- Colon tissue analysis included gross and microscopic evaluation.
- Flow cytometry assessed Treg and Th17 cell populations.
- ELISA, real-time PCR, and Western blot analyzed cytokine and protein levels.
Main Results:
- GOS treatment attenuated body weight loss and disease index in DSS-induced colitis.
- GOS ameliorated colonic histological damage.
- GOS modulated intestinal flora and corrected Th17/Treg imbalance.
- GOS significantly reduced pro-inflammatory cytokines (IL-6, IL-18, IL-13, IL-33) via NF-κB pathway inhibition.
Conclusions:
- GOS demonstrates protective effects against DSS-induced colitis.
- GOS exerts anti-inflammatory actions by regulating intestinal flora.
- The NF-κB signaling pathway is a key target for GOS's therapeutic effects in colitis.
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