Virgin Coconut Oil-Induced Neuroprotection in Lipopolysaccharide-Challenged Rats is Mediated, in Part, Through Cholinergic, Anti-Oxidative and Anti-Inflammatory Pathways

• Published in: Journal of Dietary Supplements
• Main Author: Rahim N.S.; Lim S.M.; Mani V.; Hazalin N.A.M.N.; Majeed A.B.A.; Ramasamy K.
• Format: Article
• Language: English
• Published: Taylor and Francis Ltd. 2021
• Online Access: https://www.scopus.com/inward/record.uri?eid=2-s2.0-85092504653&doi=10.1080%2f19390211.2020.1830223&partnerID=40&md5=2894b2740df19951ed1ad1c89d12efa2

Neuroinflammation is associated with neuronal cell death and could lead to chronic neurodegeneration. This study investigated the neuroprotective potential of virgin coconut oil (VCO) against lipopolysaccharide (LPS)-induced cytotoxicity of neuroblastoma SK-N-SH cells. The findings were validated using Wistar rats, which were fed with 1-10 g/kg VCO for 31 days, exposed to LPS (0.25 mg/kg) and subjected to the Morris Water Maze Test. Brain homogenate was subjected to biochemical analyses and gene expression studies. α-Tocopherol (α-T; 150 mg/kg) served as the positive control. VCO (100 µg/mL) significantly (p < 0.01) improved SK-N-SH viability (+57%) and inhibited reactive oxygen species (-31%) in the presence of LPS. VCO (especially 10 g/kg) also significantly (p < 0.05) enhanced spatial memory of LPS-challenged rats. Brain homogenate of VCO-fed rats was presented with increased acetylcholine (+33%) and reduced acetylcholinesterase (-43%). The upregulated antioxidants may have reduced neuroinflammation [malondialdehyde (−51%), nitric oxide (−49%), Cox-2 (−64%) and iNos (−63%)] through upregulation of IL-10 (+30%) and downregulation of IL-1β (-65%) and Interferon-γ (−25%). There was also reduced expression of Bace-1 (-77%). VCO-induced neuroprotection, which was comparable to α-T, could be mediated, in part, through inflammatory, cholinergic and amyloidogenic pathways. © 2020 Taylor & Francis Group, LLC.