Ginsenoside compound K up‐regulates β‐subunits of long‐chain L‐3‐hydroxyacyl‐CoA (HADHB) to promote fatty acid oxidation recovery and improve the balance of macrophage polarization in mice with ulcerative colitis

Key Points

• The aim is to explore how ginsenoside compound K affects macrophage polarization and fatty acid oxidation in ulcerative colitis.
• Examined the effects of ginsenoside compound K on macrophage polarization in mice with ulcerative colitis.
• Investigated the GR-HADHB-FAO axis related to macrophage function and fatty acid oxidation.
• Utilized biochemical assays to measure changes in polarization and metabolic pathways.
• Ginsenoside compound K up-regulated β-subunits of HADHB, promoting fatty acid oxidation recovery.
• Improved the M1/M2 macrophage balance in ulcerative colitis models was observed.
• Uncovered a novel mechanism linking ginsenoside compound K to metabolic reprogramming in macrophages.