Polysaccharide A1 from Bran-Fried Atractylodes lancea Regulates Cyclophosphamide-induced Intestinal Immune Injury in Mice via the Faecalibaculum rodentium-Mediated IAA-AHR/RORC Axis.

Authors

Wenlv Nie, Yangxin Xiao, Lijiao Zhong, Kehong Wu, Dongpeng Wang, Yanju Liu, Linghang Qu

Published in

Journal of agricultural and food chemistry. Volume 74. Issue 44. Pages 34837-34856. Nov 11, 2026.

Abstract

Cyclophosphamide-induced intestinal injury is often characterized by gut microbiota dysbiosis and metabolite imbalance. Bran-fried Atractylodes lancea polysaccharide (FALP-A1) protects against cyclophosphamide-induced intestinal injury by significantly modulating Faecalibaculum rodentium abundance. However, the mechanism of FALP-A1-mediated F. rodentium regulation remains unclear. Ex vivo digestion confirmed FALP-A1 is stable in the simulated upper gastrointestinal tract, while fermentation showed it is degradable and enriches F. rodentium. Nontargeted fecal metabolomics of in vivo mice co-treated with the FALP-A1 and Faecalibaculum rodentium, together with ex vivo coculture systems, identified Indoleacetic acid (IAA) as a potential metabolite. We further validated that IAA protects the intestinal barrier in cyclophosphamide-induced intestinal injury by modulating nuclear transcription factor RORC mRNA expression. However, these effects were reversed by an AHR inhibitor. This study elucidates the central role of "FALP-A1-F. rodentium-IAA-AHR/RORC" axis in protecting against cyclophosphamide-induced intestinal injury, providing evidence for pharmacological potential of FALP-A1 and indole-3-acetic acid.

PMID:
43012691
Bibliographic data and abstract were imported from PubMed on 11 Nov 2026.

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