Figure 6.

Molecular mechanisms of regulating NF-κB/NLRP3 pathway by ginsenosides in treating cognitive impairment in the pathological model. NF-κB pathway can be inhibited by ginsenosides via multiple ways: (1) Rf, Rb1, compound K, and Re inhibit the expression of caspase-1 to further reduce the level of IL-18 and IL-1β. (2) Rb1, compound K, and Re inhibit the expression of ASC, an important factor for formatting NLRP3 inflammasome. (3) Compound K, Re, and PF11 can directly suppress activated NLRP3 inflammasome. (4) Rg1, Rg3, Rg5, compound K, and Re downregulate the level of IL-6, TNF-α, IL-18, and IL-1β. All ginsenosides can attenuate the inflammatory state and further improve synaptic plasticity and decrease Aβ deposition and tau hyperphosphorylation.