ArticleFood science & nutrition2025
Octanoic Acid-Rich Enteral Nutrition Regulates Intestinal M1/M2 Macrophage Polarization via the PPARγ/STAT-1/STAT-6 Pathway to Alleviate Inflammatory Bowel Disease.
Article in Food science & nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Octanoic Acid-Rich Enteral Nutrition Alleviates Sepsis-Associated Metabolic Disorders by Suppressing White Adipose Tissue Browning in Mice.Food science & nutrition · 2026Article
- Nutritional Modulation of Melatonin-SIRT1 Signaling by Octanoic Acid-Rich Enteral Nutrition Protects Against Radiation-Induced Intestinal Injury.Food science & nutrition · 2026Article
- Octanoic Acid-Rich Enteral Nutrition Regulates Intestinal M1/M2 Macrophage Polarization via the PPARγ/STAT-1/STAT-6 Pathway to Alleviate Inflammatory Bowel Disease.Food science & nutrition · 2025Article
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2 authors.
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Abstract
Inflammatory bowel disease (IBD) is a complex chronic intestinal inflammatory disease involving immune, genetic and environmental interactions. A disrupted balance in the polarization of intestinal macrophages is a key pathogenic link. This study explored whether octanoic acid (OA)-rich enteral nutrition (EN) regulated intestinal M1/M2 macrophage polarization via the PPARγ/STAT-1/STAT-6 pathway to alleviate IBD. First, to assess the effects of OA-rich EN on IBD, four groups were established: the sham, IBD, IBD + EN, and IBD + OA-rich EN. Second, to verify the regulatory role of intestinal M1/M2 macrophage polarization via the PPARγ/STAT-1/STAT-6 pathway, six groups were established: the sham, IBD, IBD + OA-rich EN, IBD + OA-rich EN with intraperitoneal injections of IFNγ, AS1517499, or SR202. RAW264.7 cells were also used to observe how OA influences LPS/IFNγ-induced M1 polarization. OA-rich EN notably alleviated IBD symptoms, activated the PPARγ/STAT-1/STAT-6 pathway and remodeled the M1/M2 polarization balance of intestinal macrophages. These effects were greater than those in the IBD + EN group. Blocking the activation of PPARγ, activating STAT-1 or inhibiting STAT-6 reversed the protective effect of OA-rich EN on remodeling the M1/M2 polarization balance of intestinal macrophages and IBD symptoms. In vitro experiments further confirmed that OA regulated macrophage polarization via the PPARγ/STAT-1/STAT-6 pathway. This is the first confirmation that OA-rich EN alleviates IBD by activating PPARγ/STAT-1/STAT-6 to regulate macrophage polarization, highlighting its potential as a nutritional therapy for IBD.
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