1,3-Dichloro-2-propanol evokes inflammation and apoptosis in BV-2 microglia via MAPKs and NF-κB signaling pathways mediated by reactive oxygen species.

1,3-dichloro-2-propanol (1,3-DCP) is a widely concerned food processing contaminant which has been investigated for decades. While the neurotoxicity of 1,3-DCP and related mechanisms are still elusive. Herein, the effect of 1,3-DCP on neurotoxicity was investigated using BV-2 microglia cells. 1,3-DCP significantly decreased cell viability from 78.6% to 59.2% at doses between 2 and 20 mM. AO/EB and JC-1 staining indicated that 1,3-DCP induced apoptosis by means of the decrease of mitochondrial membrane potential. Meanwhile, western blot showed that 1,3-DCP stimulated inflammation of BV-2 cells through phosphorylation of MAPKs and activation of NF-κB pathways mediated by reactive oxygen species (ROS). Furthermore, the degree of inflammation and apoptosis has eased through MAPKs and NF-κB pathways with cells pretreated by N-acetylcysteine (NAC). Overall, these results presented here suggested that 1,3-DCP has neurotoxic effect on BV-2 microglia mainly via MAPKs and NF-κB pathways mediated by ROS.