Dietary Virgin Coconut Exerted a Neuroprotective Effect via Upregulation of Nuclear Erythroid Factor and Downregulation Of Nuclear Factor KB Expression In Acrylamide-Induced Neurotoxicity: Role Of BDNF And AchE Pathways

Acrylamide (AA), a widespread environmental neurotoxicant found in heat-processed foods, poses significant risks to neurological health. This study aimed to investigate the neuro-modulatory effects of virgin coconut oil (VCO) against AA-induced neurotoxicity in a rat model. Twenty male Wistar rats (180-250 g) were randomly divided into four groups: Control, AA (10 mg/kg), AA + 5% VCO, and AA + 10% VCO, and treated for 56 days. AA was administered orally at 10 mg/kg, with VCO incorporated into the diet at 5 g and 10 g per 100 g of normal feed. Behavioural tests demonstrated that AA exposure led to significant anxiety-like behaviour and memory deficits. Biochemical analyses revealed AA decreased serum superoxide dismutase (SOD) and catalase (CAT) activities while increasing malondialdehyde (MDA) and interleukin-1Beta (IL-1β) levels. Molecular assessments showed AA downregulated hippocampal brain-derived neurotrophic factor (BDNF) and nuclear factor erythroid 2-related factor 2 (Nrf2) and upregulated nuclear factor-κB (NF-κB) gene expression. Histological examination confirmed reduced dentate gyrus cellularity in the AA group. VCO supplementation, particularly at 5%, significantly attenuated these AA-induced alterations by restoring antioxidant enzyme activities, reducing oxidative stress and inflammation, and modulating key neuroprotective signalling pathways. These findings suggest dietary VCO supplementation can effectively mitigate AA-induced neurotoxicity through coordinated antioxidant, anti-inflammatory, and neurotrophic mechanisms.