These results suggest that EB-WE exerts its protective effects against ALI via inhibiting the activation of key signal pathways mediated by MAPKs, NF-κB, and PI3K/AKT, which induce macrophage activation in response to external stimuli [26], and down-regulating the secretion of pro-inflammatory cytokines and chemokines. Here, AKT1 is linked to acute respiratory distress syndrome.