Neuroprotective Potential of Virgin Coconut Oil in abrogating Acrylamide-induced Neurobehavioural Impairment Via NRF-2/NFK-B Signaling and BDNF Upregulation

This study investigated the effects of virgin coconut oil-supplemented diet (VCO) on acrylamide (AA)-induced neurotoxicity in Wistar rats. Twenty (20) Wistar rats (18-250g) were grouped into four (I-IV) (n = 5): I: control, received the recommended feed and water daily, II: received oral doses of AA (10 mg/kg body weight (b.w)) alone, III: received oral doses of AA (10 mg/kg b.w) and 5% VCO, IV: received oral doses of AA (10 mg/kg b.w) and 10% VCO, for 56 days. On the 55th day, the rats were subjected to behavioral tests using an elevated plus maze and Y-maze. The rats were then euthanized to obtain samples of blood for the investigation of biochemical parameters (catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), and interleukin-1B (IL-1B)) using standard methods, while the brain tissues were used for gene expressions (brain derived neurotrophic factor (BDNF), nuclear factor-erythroid factor 2-related factor 2 (NRF-2), and nuclear factor kappa-B (NFKB)). Histoarchitecture of the hippocampus to show the morphology and cell distribution of dentate gyrus was also carried out. The result revealed a significant increase in anxiety-like behaviour and memory impairment in the group that were exposed to AA only. However, administration of VCO (especially 5%) cause a significant reduction in anxiety-like behaviour and the memory impairment (p < 0.05). Similarly, AA exposure caused a significant reduction in the serum SOD and CAT (p < 0.05), increase in the serum level of MDA and IL-B. AA exposure also caused down-regulation in the gene expression levels of brain NRF-2 and BDNF, up-regulation in the gene expression level of brain NFK-B and significant decrease in the dentate gyrus cells. VCO’s administration (especially 5%) resulted in a significant increase in the serum SOD and CAT (p < 0.05), reduction in the serum level of MDA and IL-B, up-regulation in the expression of gene levels of the brain NRF-2 and BDNF, down-regulation in the gene expression level of the brain NFK-B and significant increase in the dentate gyrus cells of the hippocampus. This study concludes that VCO ameliorated AA-induced neurotoxicity via reduction of oxidative stress and inflammation.