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ORIGINAL RESEARCH article

Front. Nutr.

Sec. Nutrition and Microbes

Volume 12 - 2025 | doi: 10.3389/fnut.2025.1661040

This article is part of the Research TopicPolyphenols as Potent Modulators of Inflammation-Associated Non-Communicable DiseasesView all 3 articles

Aurantii Fructus extract alleviates DSS-induced colitis in mice via regulating NF-κB and Nrf2/HO-1 signaling pathways and modulating intestinal microbiota

Provisionally accepted
JUNBAO  YUJUNBAO YUWenya  MeiWenya MeiJiayuan  ZhuJiayuan ZhuZhihui  WangZhihui WangXiarong  LiuXiarong LiuRibao  ZhouRibao Zhou*Xiangdan  LiuXiangdan Liu*
  • Hunan University of Chinese Medicine, Changsha, China

The final, formatted version of the article will be published soon.

Ulcerative colitis (UC) is a chronic inflammatory disease that leads to a progressive loss of intestinal function. Therefore, the search for potential therapeutic agents is of great importance. This study aimed to elucidate the effects of Aurantii Fructus extract (AFE) on DSS-induced UC and intestinal microbiota. In this paper, HPLC was used to determine the components of AFE. The protective effect of AFE on UC mice was evaluated by disease activity index (DAI), colon length, and histopathological analysis. We evaluated the inflammatory status and oxidative stress by ELISA and western blotting, and the expression of tight junction proteins by immunohistochemistry. Cecal contents were used for 16S rRNA gene sequencing and analysis. The results showed that AFE treatment could alleviate the symptoms of UC mice, reduce colon damage, and restore the expression of tight junction protein ZO-1 in the colon. AFE treatment could not only reduce the levels of inflammatory factors TNF-α, IL-6 and IL-1β, inhibit the NF-κB pathway, but also increase the GSH, reduce the MDA, and activate the Nrf2/HO-1 signaling pathway. In addition, AFE treatment could inhibit the reproduction of intestinal pathogenic bacteria and restore the homeostasis of intestinal flora in UC mice, correcting the dysfunction of intestinal flora. These results indicated that AFE could alleviate DSS-induced mice UC by suppressing NF-κB, activating Nrf2/HO-1 pathways, enhancing intestinal barrier function and maintaining intestinal flora homeostasis. These findings suggest that the protective effect of AFE against DSS-induced UC may involve the inhibition of the NF-κB pathway, activation of the Nrf2/HO-1 pathway, enhanced intestinal barrier function, and the maintenance of gut microbiota homeostasis.

Keywords: Aurantii Fructus, ulcerative colitis, intestinal flora, Inflammation, Oxidative Stress

Received: 07 Jul 2025; Accepted: 30 Sep 2025.

Copyright: © 2025 YU, Mei, Zhu, Wang, Liu, Zhou and Liu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Ribao Zhou, 1057323510@qq.com
Xiangdan Liu, paeonia@hnucm.edu.cn

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