• 作者：Xun-Hu Gu^a ; ^b ; ^c ; ¹ ; Li-Jun Xu^a ; ¹ ; Zhi-Qiang Liu^a ; ^c ; Bo Wei^c ; Yuan-Jian Yang^c ; Guo-Gang Xu^d ; ^e ; Xiao-Ping Yin^a ; ^{xiaopingbuxiao@126.com" class="auth_mail" title="E-mail the corresponding author} ; Wei Wang^a ; ^{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

d="par0005">Baicalein prevents Aβ-induced impairments in hippocampal LTP through activation of Akt phosphorylation.

d="par0010">Baicalein prevents memory deficits in AD model.

d="par0015">Baicalein inhibits 12/15LO and GSK3β activity, reduces BACE1 and Aβ production, prevents tau phosphorylation, restores spine density and LTP in AD model.