In conclusion, our findings demonstrate that subacute poisoning of 1,2-DCE could stimulate microglia and astrocytes to release and produce more of the proinflammatory factor IL-1β and inflammatory mediators, including MMP-9, VCAM-1, ICAM-1, and iNOS, through the p38 MAPK/ NF-κB signaling pathway, which further induce neuroinflammatory reactions that contribute to the disruption of TJs, increase of BBB permeability and infiltration of peripheral immune cells into the brain, finally leading to brain edema in 1,2-DCE-intoxicated mice. The gene discussed is NOS2; the disease is edema.