ArticleEuropean journal of nutrition2025
Ellagic acid alleviates DSS-induced ulcerative colitis by inhibiting ROS/NLRP3 pathway activation and modulating gut microbiota in mice.
Article in European journal of nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Optimization of Ellagic Acid-Loaded Liposomes Using Box-Behnken Design and the Modulatory Role of Chitosan Molecular Weight on Their Stability, Digestive Release, and Antioxidant Activity.Foods (Basel, Switzerland) · 2026Article
- Therapeutic Potential of Kinkeliba (Molecules (Basel, Switzerland) · 2026Article
- Identification of Ellagic Acid as a Natural GPR35 Agonist for Ulcerative Colitis Therapy.Biomolecules · 2026Article
- Therapeutic Agents Targeting the Nrf2 Signaling Pathway to Combat Oxidative Stress and Intestinal Inflammation in Veterinary and Translational Medicine.Veterinary sciences · 2025Review
- Effects of the Brazilian Native Fruit Jaboticaba (Foods (Basel, Switzerland) · 2025Article
- Ulceroprotective Effects ofCurrent issues in molecular biology · 2025Article
- Berberine-taxifolin co-administration attenuates inflammatory response and intestinal barrier injury via nf-κB/NLRP3 suppression in colitis.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Ulcerative colitis (UC) can cause severe oxidative stress in the colon, which can lead to tissue damage and an imbalance in the normal gut microbiota. Ellagic acid (EA) is one of the main types of plant polyphenols with improved pharmacological effects such as antioxidant, anti-inflammatory, and antibacterial properties. However, currently, the studies on the impact of EA on the gut microbiota and its potential to alleviate UC in mice through the ROS/NLRP3 pathway are limited. In this study, dextran sodium sulfate (DSS) was used to construct a UC mouse model, which was then treated with EA as an intervention for UC. The results revealed that EA alleviated the trend of liver, spleen, and weight changes in UC mice and improved colon oxidative stress, inflammation, and pathological damage. Mechanistically, DSS-induced UC indicated a significant increase in ROS/NLRP3 pathway-related factors, whereas EA intervention activated the Nrf2 pathway to reduce these factors. Furthermore, the DSS group had a reduced abundance of Firmicutes (59.02%) and an increased abundance of Bacteroides and Proteobacterium by 1.8 times and 10.16%; however, EA intervention reversed these changes, thus alleviating UC. The findings of this study revealed that EA could significantly enhance the composition of gut microbiota in UC and reduce the inflammatory response, colonic damage as well as oxidative stress caused by DSS by regulating the ROS/NLRP3 pathway. These results provide novel perspectives on the prevention and treatment strategies of UC and highlight the therapeutic benefits of EA in managing colitis.
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Registered trials
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