Lipoic acid prevents acrylamide-induced neurotoxicity in CD-1 mice and BV2 microglial cells via maintaining redox homeostasis

Acrylamide (ACR) is known as a contaminant generated in starchy foods during cooking at high-temperature. In this study, pre-treatment with LA improved gait abnormalities and mnemonic and exploration ability of CD-1 male mice administrated with ACR. Alleviative effect of LA was further observed on histological damage, cell death and suppression of brain derived neurotrophic factor (BDNF), nerve terminal factors (NSF) in ACR-treated mice brain. LA pretreatment was confirmed to confer protection through its redox modulation in cell signaling and transcription towards glial activation and inflammatory responses triggered by ACR. Concomitantly, LA pretreatment abolished ACR-stimulated mitochondrial dysfunction and cell death in BV2 microglial cells, accompanied with the suppression of myeloperoxidase (MPO) over-activation, enhancement in glutathione (GSH) level and BDNF expression in BV2 microglial cells. Overall, LA maintained redox homeostasis in brain, restrained microglial excessive activation and the subsequent MPO over-expression, thus ameliorated ACR-triggered neurotoxicity and cognitive impairments.