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

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 ant...

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Published in:European Journal of Nutrition Vol. 64; no. 1; pp. 1 - 18
Main Authors: Xiong, Yanling, Cheng, Zhentao, Zhang, Yangzi, Liu, Ting, Wan, Zhiling, Xia, Cuiyun, Zhou, Binlan, Shan, Chunlan, Song, Derong, Miao, Fujun
Format: Journal Article
Published: Springer Nature Feb2025
Online Access:View this record in EBSCOhost
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      jtl: European Journal of Nutrition
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      dt: Feb2025
      vid: 64
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      pub: Springer Nature
      place: New York, New York
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        182106356
        10.1007/s00394-024-03577-7
        182106356
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        atl: Ellagic acid alleviates DSS–induced ulcerative colitis by inhibiting ROS/NLRP3 pathway activation and modulating gut microbiota in mice.
      aug:
        au:
          Xiong, Yanling
          Cheng, Zhentao
          Zhang, Yangzi
          Liu, Ting
          Wan, Zhiling
          Xia, Cuiyun
          Zhou, Binlan
          Shan, Chunlan
          Song, Derong
          Miao, Fujun
        affil: https://ror.org/02wmsc916 College of Animal Science, Guizhou University, 550000, Guiyang, People’s Republic of China
      sug:
      ab: 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.
      pubtype: Academic Journal
      doctype: Journal Article
      ougenre: Article
    language: English
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