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Schisandrin a Alleviates Ulcerative Colitis by Modulating Gut Microbiota and ALOX15-Mediated Ferroptosis
Zhuosi Chen1, Guixuan Fang1, Yulu Zhao1
1The Marine Biomedical Research Institute of Guangdong Zhanjiang, School of Ocean and Tropical Medicine Guangdong Medical University, Zhanjiang, Guangdong 524023, China.
Journal of Agricultural and Food Chemistry
|June 29, 2026
Summary
Schisandrin A, a natural compound, effectively treats ulcerative colitis (UC) by restoring gut microbiota and blocking ferroptosis. This research highlights Schisandrin A as a potential new therapy for inflammatory bowel disease (IBD).
Area of Science:
- Gastroenterology
- Pharmacology
- Microbiology
Background:
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) with limited treatment options.
- Natural therapeutic candidates are needed for refractory UC.
- Schisandrin A (Sch A) is a bioactive lignan with potential therapeutic properties.
Purpose of the Study:
- To investigate the efficacy of Schisandrin A (Sch A) in a mouse model of dextran sulfate sodium (DSS)-induced UC.
- To elucidate the underlying mechanisms of Sch A's protective effects against UC.
Main Methods:
- DSS-induced UC mouse model.
- 16S rRNA sequencing for gut microbiota analysis.
- In vivo and in vitro ferroptosis assays.
- Multiomics analyses to identify molecular targets.
- Molecular docking, MD simulations, CETSA, and DARTS to confirm target binding.
Main Results:
- Sch A significantly repaired colonic barrier function in UC mice.
- Sch A remodeled gut microbiota, increasing probiotics and decreasing pathogens.
- Sch A suppressed ferroptosis both in vivo and in vitro.
- ALOX15 was identified as a core target, with direct binding confirmed between Sch A and ALOX15.
Conclusions:
- Schisandrin A alleviates UC by modulating gut microbiota and inhibiting ferroptosis.
- Targeting ALOX15 is a key mechanism for Sch A's therapeutic effect in UC.
- Sch A represents a promising food-derived agent for UC therapy.
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