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Deoxyschizandrin attenuates Aβ1–42-induced cognitive impairments through up-regulation of AMPA receptors in mice

Yan, Tingxu, Xu, Mengjie, Wan, Shutong, Wu, Bo, Xiao, Feng, Bi, Kaishun, Jia, Ying
Phytochemistry letters 2018 v.28 pp. 24-31
acetylcholinesterase, cognition, cognitive disorders, cortex, enzyme inhibition, frontal lobe, hippocampus, histology, males, mice, neurons, receptors
The present study was undertaken to investigate the possible effect of deoxyschizandrin (DSD) on improving cognitive impairment in mice induced by β-amyloid (Aβ). The Aβ1-42 was injected into the hippocampus of male mice and the mice were treated by DSD (0.01 or 0.1 mg/kg) or their vehicles into the lateral ventricle until the start of behavioral tests. The cognitive improvement effect was assessed by the Y-maze, shuttle box and the Morris water maze test. The changes in the levels of AMPA receptors (GluR1 and GluR2), amounts of β-secretase and acetyl cholinesterase (AChE) in the cortex and hippocampus were detected. Moreover, hippocampus neurons in the CA1 subfield were examined. The results showed that intracerebroventricular (i.c.v.) administration of DSD (0.1 mg/kg) significantly reversed cognitive impairments induced by Aβ1-42 in mice. Remarkably, DSD (0.1 mg/kg, i.c.v.) was found to decrease the levels of AChE and β-secretase in hippocampus and frontal cortex, respectively. in addition to increasing the expressions both in GluR1 and GluR2. These results demonstrated DSD could improve the behavioral disorders, inhibit β-secretase and restore AChE, glutamate, synaptic dysfunction and loss induced by Aβ1-42. Moreover, the histology assay in the hippocampus of mice indicated that the neurotrophic effects of DSD.