Anti-inflammation was firstly found in the NBP-treated stroke model; NBP enhanced the proliferation of microglia and promoted the microglia polarization into M2 phenotype, an anti-inflammation phenotype, by activating the calcium/calmodulin-dependent protein kinase β (CaMKKβ)-AMPK pathway or PPARγ nuclear translocation; NBP also decreased the infiltration of endothelial cells by downregulating intercellular adhesion molecule 1 (ICAM-1) and protease-activated receptor-1 (PAR-1) (Zeng et al., 2020; Liu et al., 2021b). This evidence concerns the gene ICAM1 and Stroke.