Abstract

In addition, FEH treatment increased ACh and BDNF levels, and reduced the levels of IL-1β, TNF-α and IL-6 in brain hippocampal tissue of mice with scopolamine-induced memory and learning impairment. Furthermore, FEH treatment enhanced the expression of phosphorylated cAMP response element-binding protein (p-CREB) and BDNF via the stimulation of the phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin/postsynaptic density protein 95 (p-PI3K/p-AKT/mTOR/PSD95) pathway, and activation of Extracellular Signal-Regulated Kinases (ERK) and Ca2+/calmodulin-dependent protein kinase II (CaMKII). These results provide extensive information regarding the protective mechanism of action of FEH, and support the potential of FEH supplementation to prevent learning and memory impairment.

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