Dietary broccoli alleviates intestinal inflammation in mice by mitigating ferroptosis induced through activating AhR
The aryl hydrocarbon receptor (AHR) is a versatile transcription factor, that responds to a diverse array of both exogenous and endogenous ligands. Broccoli consumption was shown to alter the microbiota, and attenuate chemically induced colitis in mice through AhR-dependent pathway. The study highlights the important role that dietary aryl hydrocarbon receptor (AHR) ligands play in maintaining the mucus barrier's homeostasis. The absence of AHR ligands in the diet causes a distinct alteration of the mucinous component that potentially increased the susceptibility to colitis by decreasing acidic mucin and lysozyme levels. The research identifies ferroptosis-induced endoplasmic reticulum (ER) stress as a probable contributing factor to the adjustment of mucin-2 (MUC-2) levels. Overall, our study presents a novel approach to improving the nutraceutical quality of Brassicaceae, while also offering fresh insights into the impacts of cruciferous vegetables on intestinal health in humans. • The dietary AHR ligands of broccoli are crucial for mucus barrier homeostasis. • AHR-rich diet suppresses ferroptosis with upregulation of SLC7A11/GPX4 axis. • Ferroptosis-induced hypersecretion of mucus levels contributes to ER stress during colitis. • AHR activation deficiency reshaped the gut microbiome, increasing Faecalibaculum and Akkermansia muciniphila abundance.
Authors
- Jia-ming Yang
- Zeyu Gao (ORCID: https://orcid.org/0000-0003-2365-8318)
- Yuanfang Chen (ORCID: https://orcid.org/0000-0002-1109-8491)
- Ze Bo Hu
- Haikang Tang
- Wenqing Xu (ORCID: https://orcid.org/0000-0003-0163-2870)
- Xiaoliang Zhuo
Institutions
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
Publication Details
- Journal
- Journal of Functional Foods
- Published
- 2025-03-29
- DOI
- https://doi.org/10.1016/j.jff.2025.106770
- Citations
- 1
- Primary Topic
- Ferroptosis and cancer prognosis
- Type
- article
- Field-Weighted Citation Impact
- 1.52