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. (1st March 2018)

• Record Type: Journal Article
• Authors: Xiao, Chunxia; He, Pandi; Han, Jingjing; Tang, Miaoling; Wang, Zhen; Mi, Yashi; Liu, Xuebo
• Is Part Of: Toxicology letters. Volume 284(2018)
• Page Start: 103
• Page End: 112
• Publication Date: 2018-03-01
• Subjects: 1, 3-DCP 1, 3-dichloro-2-propanol -- BV-2 cell mouse microglia cell line -- COX-2 cyclooxygenase-2 -- AO acridine orange -- EB ethidium bromide -- NO nitric oxide -- iNOS inducible nitric oxide synthase -- ROS reactive oxygen species -- GSH glutathione -- NAC N-Acetylcysteine -- PDTC pyrrolidine dithiocarbamate -- DCFH-DA 2′, 7′-dichlorofluorescin diacetate -- NF-κB nuclear factor κB -- MTT 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide -- MAPKs mitogen-activated protein kinases; 1, 3-DCP -- Neurotoxicity -- ROS -- MAPKs -- NF-κB; Toxicology -- Periodicals; 363.179
• DOI: 10.1016/j.toxlet.2017.12.011
• Languages: English
• ISSNs: 0378-4274

Abstract

Graphical abstract: Highlights: The neurotoxic effect of 1, 3-DCP on BV-2 microglia is proposed. 1, 3-DCP induces apoptosis and inflammation in BV-2 cells. The mechanism of apoptosis relies on cyt C release and activation of caspases. The inflammation induced by 1, 3-DCP is via MAPKs and NFκB pathways mediated by ROS. Abstract: 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.