They could restrain the activation and polarization of microglia, as well as inhibit the expression of pro-inflammatory mediators via suppressing NLRP3 inflammasome activation and regulating PI3k/Akt, MAPKs, Nrf2 or NF-κB signaling pathways in PD, AD, traumatic brain injury, depression and I/R injury, which are specifically showed in Table 1. This evidence concerns the gene NFKB1 and Alzheimer disease.