Abstract
Chlorpyrifos (CPF) is an organophosphorus pesticide that can damage the central nervous system in children upon exposure. Taxifolin (Tax) exerts protective effects against neurotoxins; however, the mechanism has not yet been illustrated. The current study used BV2 cells to investigate the protective mechanism underlying the organophosphorus pesticide taxifolin on CPF-induced neurotoxicity, which might present a therapeutic potential for the prevention and treatment of the nervous system diseases in children. BV2 cells were randomly divided into 4 groups: DMSO, CPF, Tax, and Tax + CPF. The viability, morphocytology, oxidative stress, inflammatory reaction, and autophagocytosis have been studied in the cells using Western blot analysis, CCK-8 assay, enzyme-linked immunosorbent assay, and immunofluorescence to estimate the level of LC3 II. As a result, CPF was found to exert a significant toxic effect on BV2 cells that was characterized by rounded cell body, atrophic synapse, poor adhesion, cell aggregation, inflammation, oxidative reaction, and autophagy. Tax treatment has a protective effect on CPF-induced neurotoxicity via downregulation of ROS, TNF-α, IFN-γ, and p62 levels and increased LC3 II level, which in turn, improved the viability and activity of BV2 cells. This phenomenon suggested that Tax can reduce the inflammation and oxidative stress and promote autophagy. Furthermore, the current study suggested that the protective mechanism of Tax on CPF-induced BV2 cell toxicity was via up-regulation of pAMPK level and activation of Nrf2/HO-1 signaling pathway.