Ginsenoside Rb1 exerts anti-inflammatory effects in vitro and in vivo by modulating toll-like receptor 4 dimerization and NF-kB/MAPKs signaling pathways.

Ginsenoside Rb1 significantly exhibits an anti-inflammatory effect. Rb1 decreases inflammatory cytokine release in LPS-stimulated RAW264.7 cells and BMDMs. The NF-κB and MAPK axes participate in Rb1’s anti-inflammatory effects. Molecular docking simulation indicates that Rb1 binds to TLR4 to prevent TLR4 dimerization, as confirmed by co-immunoprecipitation and cellular thermal shift assay. Furthermore, MyD88 recruitment and TAK1 expression are altered by reduced TLR4 dimerization, indicating the TLR4-MyD88-NF-κB/MAPK pathways contribute to Rb1’s anti-inflammatory process. Image, graphical abstract