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

This is the authors' abstract. We don't add key points for this paper.

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.