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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.