This study aimed to investigate the ameliorating effect of an
ethyl acetate fraction from the fruit Actinidia arguta (EFAA) on
amyloid beta (Aβ)-induced neurotoxicity and cognitive deficits in ICR mice. EFAA showed potent protective effects against Aβ-induced neurotoxicity through
2',7'-dichlorofluorescein diacetate (DCF-DA), 2',3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium
bromide (MTT) and
lactate dehydrogenase (LDH) release into the assay medium. EFAA treatment reduced the intracellular ROS level and
lactate dehydrogenase (LDH) release in the mitochondria, and increased cell viability in Aβ-induced
neuroblastoma MC-IXC cells. The administration of EFAA significantly attenuated Aβ-induced learning and
memory deficits, which were evaluated by Y-maze, passive avoidance, and Morris water maze tests. Furthermore, EFAA showed the ameliorating effect of
cholinergic functions by increasing
acetylcholine (ACh) levels and decreasing
acetylcholinesterase (AChE) activity, and protected
antioxidant systems by increasing
superoxide dismutase (SOD) and decreasing the
oxidized glutathione (GSH)/total GSH and
malondialdehyde (MDA) in the brain. Finally, EFAA prevented
mitochondrial dysfunction via regulating apoptotic signaling molecules including phosphorylated Akt (p-Akt), phosphorylated tau (p-tau), Bax, and
cytochrome c in the brain tissues. Therefore, the present study suggests that EFAA might be a potential source of natural
antioxidants with the ability to ameliorate Aβ-induced
amnesia.