Anti-inflammatory effects of ginsenoside compound K in ethanol-stimulated macrophages by modulating sirtuin 1

• Published in: Journal of functional foods 2024-06, Vol.117, p.106218, Article 106218
• Main Authors: Gwon, Yubin, Moon, Chae Young, Lee, Eun-Ho, Im, Seung-Soon, Kang, Hyunju
• Format: Article
• Language: English
• Subjects: Estrogen receptor α; Ginsenoside compound K; Inflammation; Macrophage; Sirtuin 1
• ISSN: 1756-4646; 2214-9414
• DOI: 10.1016/j.jff.2024.106218

[Display omitted] •GCK mitigates inflammation and oxidative stress in ethanol-exposed macrophages.•GCK restores SIRT1 and NAD+ salvage pathway in ethanol-stimulated macrophages.•GCK ameliorates ethanol-induced metabolic alterations in macrophages.•GCK attenuates ethanol-triggered changes in macrophages via SIRT1 and ERα. Inflammatory responses by macrophages have been pivotal in the pathogenesis of various diseases. We previously demonstrated the anti-inflammatory effects of ginsenoside compound K (GCK) through sirtuin 1 (SIRT1) activation in lipopolysaccharide-treated macrophages. This study extended the efficacy of GCK in mitigating ethanol-induced inflammation in macrophages through the interplay between SIRT1 and estrogen receptor α (ERα). Ethanol elevated inflammatory and oxidative stress genes with reduced SIRT1 expression. GCK reversed these effects, concomitantly inhibiting M1 polarization in macrophages. The efficacy of GCK in modulating ethanol-altered glycolysis and NAD+ salvage pathway was demonstrated through its interaction with SIRT1 and ERα. Activation of SIRT1 by GCK leads to the activation of ERα, and vice versa, suggesting a synergistic relationship between SIRT1 and ERα mediated by GCK. In conclusion, GCK exhibited anti-inflammatory and antioxidant properties, which may counteract energy metabolism disruptions in ethanol-stimulated macrophages, through the interplay between SIRT1 and ERα.