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Updated: Nov 11, 2025

Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
Pristimerin reduces dextran sulfate sodium-induced colitis in mice by inhibiting microRNA-155
Minxiu Tian1, Shuai Peng2, Shanshan Wang2
1Renmin Hospital of Wuhan University, Hubei Key Laboratory of Digestive System Disease, Wuhan 430060, Hubei Province, China.
Abstract:
Pristimerin (Pris), which is a natural triterpenoid compound extracted from the Celastraceae plant, has an effect on intestinal inflammation, but its mechanism needs further study. Human genome-wide analysis found that the expression of microRNA-155 in the blood and colon tissue of patients with IBD was increased. Therefore, we studied the effect of Pris on a model of DSS-induced colitis in mice and investigated whether Pris inhibited the expression of microRNA-155. We obtained a mouse model of acute experimental colitis by allowing the mice to drink a 3% by mass DSS solution freely for 7 days. Pris solutions at different concentrations were injected via the abdomen to simulate the therapeutic effect of Pris on colitis. The body weight and faeces were measured and recorded daily. The mice were sacrificed by the cervical dislocation method after the experiment, and the colon length and histological changes, as well as the changes in Nrf2 in the colon tissue, were measured. The activities of the antioxidant enzymes GSH, GSH-Px and SOD were examined. The expression levels of microRNA-155, IL-1β, IL-6, IL-17, and TNF-α in the colon were detected by RT-PCR technology, and the expression of NF-κB p65 in the colon was detected by western blotting. Our study shows that Pris can reduce the DAI score, obviously alleviate weight loss, and decrease the colon pathological tissue damage caused by DSS. Pris can inhibit the increase in microRNA-155 expression induced by DSS-induced colitis. Our study has shown that Pris may reduce DSS-induced colitis in mice by inhibiting the expression of microRNA-155, and further inhibition of the inflammatory response and oxidative stress occurred.
Insights
Pristimerin (Pris) reduces intestinal inflammation in a mouse model of colitis. This natural compound inhibits microRNA-155, thereby decreasing inflammatory responses and oxidative stress.
Area of Science:
- Pharmacology
- Gastroenterology
- Molecular Biology
Background:
- Inflammatory bowel disease (IBD) is characterized by increased microRNA-155 expression.
- Pristimerin (Pris), a natural triterpenoid, shows potential in treating intestinal inflammation.
- The precise mechanism of Pris in IBD requires further elucidation.
Purpose of the Study:
- To investigate the therapeutic effect of Pris on dextran sulfate sodium (DSS)-induced colitis in mice.
- To determine if Pris inhibits microRNA-155 expression in the context of colitis.
- To explore the impact of Pris on inflammatory and oxidative stress pathways.
Main Methods:
- A mouse model of acute experimental colitis was induced using 3% DSS.
- Mice were treated with varying concentrations of Pris via abdominal injection.
- Disease activity index (DAI), body weight, fecal characteristics, colon length, histology, and molecular markers (microRNA-155, inflammatory cytokines, Nrf2, antioxidant enzymes, NF-κB p65) were assessed.
Main Results:
- Pris treatment significantly reduced DAI scores, alleviated weight loss, and mitigated colon pathological damage.
- Pris effectively inhibited the DSS-induced upregulation of microRNA-155 expression in colon tissue.
- Pris treatment led to the inhibition of inflammatory responses and oxidative stress markers.
Conclusions:
- Pristimerin demonstrates significant therapeutic potential for DSS-induced colitis in mice.
- Inhibition of microRNA-155 appears to be a key mechanism by which Pris exerts its anti-inflammatory and anti-oxidative effects.
- These findings suggest Pris as a promising candidate for IBD treatment.
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