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Virgin coconut oil (VCO) by normalizing NLRP3 inflammasome showed potential neuroprotective effects in Amyloid-β induced toxicity and high-fat diet fed rat

Mirzaei, Fatemeh, Khazaei, Mozafar, Komaki, Alireza, Amiri, Iraj, Jalili, Cyrus
Food and chemical toxicology 2018 v.118 pp. 68-83
Alzheimer disease, blood sampling, coconut oil, heart, high fat diet, hippocampus, hyperlipidemia, immunohistochemistry, inflammasomes, laboratory animals, males, memory, models, neuroprotective effect, oxidative stress, rats, staining, surgery, toxicity, toxicology
Both dyslipidemia and Alzheimer disease (AD) are associated with aging. In this study, the effects of virgin coconut oil (VCO) on inflammasome and oxidative stress in Alzheimer's model (receiving Amyloid-β (Aβ)) and high-fat diet (HFD) model were determined. A total of 120 male Wistar rats, were divided into 12 groups (n = 10), including; healthy control, sham surgery, sham surgery receiving normal saline, HFD, HFD + 8% VCO, HFD + 10% VCO, Aβ received rats, Aβ + 8%VCO, Aβ + 10%VCO, HFD + Aβ, HFD + Aβ+8%VCO, and HFD + Aβ + 10%VCO. Following memory and learning tests, blood sample prepared from the heart and hippocampus of rats in each group was kept at −70 °C for genes expression, oxidative stress, and biochemical tests. Aβ and HFD significantly impaired memory and learning by activating of both NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and oxidative stress (p<0.05), while treatment with both 8 and 10% VCO normalized inflammasome genes expression and oxidative stress (p<0.05). The Congo Red, Cresyl Violet staining and immunohistochemistry (IHC) test revealed that VCO improved hippocampus histological changes, reduced Aβ plaques and phosphorylated Tau. High-fat diet has exacerbated the effects of Aβ, while VCO showed potential neuroprotective effect.