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Ellagic acid alleviates DSS-induced ulcerative colitis by inhibiting ROS/NLRP3 pathway activation and modulating gut microbiota in mice

文献类型： 外文期刊

作者： Xiong, Yanling 1 ; Cheng, Zhentao 1 ; Zhang, Yangzi 2 ; Liu, Ting 1 ; Wan, Zhiling 1 ; Xia, Cuiyun 1 ; Zhou, Binlan 1 ; Shan, Chunlan 1 ; Song, Derong 3 ; Miao, Fujun 4 ;

作者机构： 1.Guizhou Univ, Coll Anim Sci, Guiyang 550000, Peoples R China

2.Guizhou Acad Agr Sci, Inst Biol, Guiyang 550001, Peoples R China

3.Bijie Inst Anim Husb & Vet Sci, Bijie 551700, Peoples R China

4.Yunnan Acad Forestry & Grassland, Kunming 650204, Peoples R China

关键词： Ellagic acid; Ulcerative colitis; Oxidative stress; ROS/NLRP3 pathway; Gut microbiota

期刊名称：EUROPEAN JOURNAL OF NUTRITION （ 影响因子：4.3； 五年影响因子：4.7 ）

ISSN： 1436-6207

年卷期： 2025 年 64 卷 1 期

页码：

收录情况： SCI

摘要： 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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