Abstract
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.
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