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Peer-reviewedCC BY 4.0Cell Reports Medicine

Microbiota-mediated naringenin release limits postoperative acute gastrointestinal injury by suppressing ferroptosis

  • Fan Deng1,2
  • Jingjuan Hu1,2
  • Yue Min1,2
  • Sun Xie1,2
  • Zebin Lin1,2
  • Qishun Sun1,2
  • Huamin Liu1,2
  • Shiying He1,2
  • Siyuan Feng1,2
  • Ling Wu1,2
  • Xiaofeng Chen1,2
  • Linghong Xu1,2
5 more authors
  • Zheang Zhang1,2
  • Wenqi Tang1,2
  • Zhuang Li3
  • Hongwei Zhou3,4,5
  • Kexuan Liu1,2
5 affiliations
  1. 1Department of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China
  2. 2Guangdong Provincial Key Laboratory of Precision Anesthesia and Perioperative Organ Protection, Guangzhou, Guangdong, China
  3. 3Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, China
  4. 4Shenzhen Key Laboratory of Gastrointestinal Microbiota and Disease, Department of Gastroenterology, Gynecology and Obstetrics, and Laboratory Medicine, Shenzhen Hospital, Southern Medical University, Shenzhen, Guangdong, China
  5. 5State Key Laboratory of Multi-organ Injury Prevention and Treatment, Southern Medical University, Guangzhou, China
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Abstract

Acute gastrointestinal injury (AGI) remains a major complication after cardiopulmonary bypass, yet its microbiome-related determinants are unclear. We identify microbiota-mediated naringenin (NAR) release as a candidate modulator of AGI susceptibility. Patients who subsequently develop AGI have lower preoperative fecal NAR levels and β-glucuronidase (GUS) activity, accompanied by reduced abundance of Bacteroides vulgatus (B. vulgatus). In germ-free and conventional mice, B. vulgatus alleviates intestinal ischemia-reperfusion injury through GUS-dependent release of NAR from its glucuronide conjugate. Mechanistically, NAR engages the TLR4/MyD88-SPRR2A axis to suppress CHAC1-driven ferroptosis, thereby maintaining epithelial integrity and promoting mucosal repair in vivo and in organoids. Clinically, preoperative fecal NAR concentration and GUS activity show exploratory value as noninvasive markers for postoperative AGI risk stratification. Collectively, these findings support a microbiota-host metabolic model in which microbial NAR release may mitigate postoperative gastrointestinal injury by restricting ferroptosis, with potential implications for risk assessment and therapeutic modulation.

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Cite

BibTeXRIS
BibTeX
@article{deng2026microbiotamediated,
  title = {{Microbiota-mediated naringenin release limits postoperative acute gastrointestinal injury by suppressing ferroptosis}},
  author = {Fan Deng and Jingjuan Hu and Yue Min and Sun Xie and Zebin Lin and Qishun Sun and Huamin Liu and Shiying He and Siyuan Feng and Ling Wu and Xiaofeng Chen and Linghong Xu and Zheang Zhang and Wenqi Tang and Zhuang Li and Hongwei Zhou and Kexuan Liu},
  journal = {Cell Reports Medicine},
  year = {2026},
  month = oct,
  doi = {10.1016/j.xcrm.2026.103101},
  url = {https://doi.org/10.1016/j.xcrm.2026.103101},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Microbiota-mediated naringenin release limits postoperative acute gastrointestinal injury by suppressing ferroptosis
AU  - Fan Deng
AU  - Jingjuan Hu
AU  - Yue Min
AU  - Sun Xie
AU  - Zebin Lin
AU  - Qishun Sun
AU  - Huamin Liu
AU  - Shiying He
AU  - Siyuan Feng
AU  - Ling Wu
AU  - Xiaofeng Chen
AU  - Linghong Xu
AU  - Zheang Zhang
AU  - Wenqi Tang
AU  - Zhuang Li
AU  - Hongwei Zhou
AU  - Kexuan Liu
PY  - 2026
DA  - 2026/10/08
JO  - Cell Reports Medicine
DO  - 10.1016/j.xcrm.2026.103101
UR  - https://doi.org/10.1016/j.xcrm.2026.103101
AB  - Acute gastrointestinal injury (AGI) remains a major complication after cardiopulmonary bypass, yet its microbiome-related determinants are unclear. We identify microbiota-mediated naringenin (NAR) release as a candidate modulator of AGI susceptibility. Patients who subsequently develop AGI have lower preoperative fecal NAR levels and β-glucuronidase (GUS) activity, accompanied by reduced abundance of Bacteroides vulgatus (B. vulgatus). In germ-free and conventional mice, B. vulgatus alleviates intestinal ischemia-reperfusion injury through GUS-dependent release of NAR from its glucuronide conjugate. Mechanistically, NAR engages the TLR4/MyD88-SPRR2A axis to suppress CHAC1-driven ferroptosis, thereby maintaining epithelial integrity and promoting mucosal repair in vivo and in organoids. Clinically, preoperative fecal NAR concentration and GUS activity show exploratory value as noninvasive markers for postoperative AGI risk stratification. Collectively, these findings support a microbiota-host metabolic model in which microbial NAR release may mitigate postoperative gastrointestinal injury by restricting ferroptosis, with potential implications for risk assessment and therapeutic modulation.
SN  - 2666-3791
ER  -