The flavonoid baicalein rescues synaptic plasticity and memory deficits in a mouse model of Alzheimer’s disease
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- 作者：Xun-Hu Gua ; b ; c ; 1 ; Li-Jun Xua ; 1 ; Zhi-Qiang Liua ; c ; Bo Weic ; Yuan-Jian Yangc ; Guo-Gang Xud ; e ; Xiao-Ping Yina ; xiaopingbuxiao@126.com" class="auth_mail" title="E-mail the corresponding author ; Wei Wanga ; wuhansy@126.com" class="auth_mail" title="E-mail the corresponding author
- 关键词：AD ; Alzheimer&rsquo ; s disease ; ACSF ; artificial cerebrospinal fluid ; Akt ; serine threonine Kinase ; APP ; amyloid precursor protein ; Aβ ; β-amyloid ; BACE1 ; β-secretase enzyme ; Bai ; baicalein ; fEPSP ; field excitatory postsynaptic potential ; GluR1 ; α-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) receptor subunit 1 ; GSK3β ; glycogen synthase kinase 3β ; HFS ; high-frequency stimulation ; LTP ; long-term potentiation ; NMDAR ; N-methyl-d-aspartate receptor ; NR1 ; NMDA receptor subunit 1 ; NR2A ; NM
- 刊名：Behavioural Brain Research
- 出版年：2016
- 出版时间：15 September 2016
- 年：2016
- 卷：311
- 期：Complete
- 页码：309-321
- 全文大小：3454 K
文摘
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Baicalein prevents Aβ-induced impairments in hippocampal LTP through activation of Akt phosphorylation.
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Baicalein prevents memory deficits in AD model.
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Baicalein inhibits 12/15LO and GSK3β activity, reduces BACE1 and Aβ production, prevents tau phosphorylation, restores spine density and LTP in AD model.