IR@PKUHSC  > 北京大学第一临床医学院
学科主题临床医学
Icariin attenuates beta-amyloid-induced neurotoxicity by inhibition of tau protein hyperphosphorylation in PC12 cells
Zeng, Ke-Wu1,2; Ko, Hyeonseok1; Yang, Hyun Ok1; Wang, Xue-Mei2
关键词Icariin Beta-amyloid (a Beta) Tau Protein Hyperphosphorylation Gsk-3 Beta Pi3k/akt
刊名NEUROPHARMACOLOGY
2010-11-01
DOI10.1016/j.neuropharm.2010.07.020
59期:6页:542-550
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Neurosciences ; Pharmacology & Pharmacy
研究领域[WOS]Neurosciences & Neurology ; Pharmacology & Pharmacy
关键词[WOS]GLYCOGEN-SYNTHASE KINASE-3 ; ALZHEIMERS-DISEASE ; OKADAIC ACID ; ENDOTHELIAL-CELLS ; CORTICAL-NEURONS ; IN-VITRO ; PHOSPHORYLATION ; GSK-3-BETA ; BRAIN ; GLYCOGEN-SYNTHASE-KINASE-3
英文摘要

Alzheimer′s disease (AD) is a neurodegenerative disease characterized by the progressive loss of neurons and production of beta-amyloid proteins (A beta). Hyperphosphorylation of tau protein is proposed to be an early event for the evolution of AD, and may play an important role in A beta-induced neurodegeneration. Icariin, a flavonoid compound from the herb Epimedium brevicornum Maxim, exerts a protective effect on learning and memory abilities in A beta(25-35)-induced AD rats. However, the molecular mechanism of icariin-induced neuroprotective effect against tau protein hyperphosphorylation, which is one of the most representative hallmarks in AD, is still unknown. In the present study, we investigated the inhibitory effect of icariin on A beta(25-35)-induced tau protein hyperphosphorylation on PC12 cells. The results showed that treatment with icariin significantly decreased A beta(25-35)-induced cytotoxity and apoptosis rate through inhibiting tau protein hyperphosphorylation at Ser396, Ser404 and Thr205 sites, respectively. Mechanism study showed that icariin could activate PI3K/Akt signaling pathway, resulting in an inhibitory effect on glycogen synthase kinase (GSK)-3 beta, which is an important kinase response for tau protein hyperphosphorylation in the development of AD. These observations indicate that icariin is capable of attenuating A beta(25-35)-induced tau protein hyperphosphorylation and promoting survival of neuronal cells, meanwhile also provide some insights into the potential signaling pathway that is involved. Thus, this study promises a great potential agent for Alzheimer′s disease and other tau pathology-related neuronal degenerative diseases. (C) 2010 Elsevier Ltd. All rights reserved.

语种英语
WOS记录号WOS:000283453300023
Citation statistics
Cited Times:51[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56850
Collection北京大学第一临床医学院
作者单位1.Peking Univ, Hosp 1, Beijing 100034, Peoples R China
2.Korea Inst Sci & Technol, Gangneung Inst, Nat Prod Res Ctr, Kangnung 210340, South Korea
Recommended Citation
GB/T 7714
Zeng, Ke-Wu,Ko, Hyeonseok,Yang, Hyun Ok,et al. Icariin attenuates beta-amyloid-induced neurotoxicity by inhibition of tau protein hyperphosphorylation in PC12 cells[J]. NEUROPHARMACOLOGY,2010,59(6):542-550.
APA Zeng, Ke-Wu,Ko, Hyeonseok,Yang, Hyun Ok,&Wang, Xue-Mei.(2010).Icariin attenuates beta-amyloid-induced neurotoxicity by inhibition of tau protein hyperphosphorylation in PC12 cells.NEUROPHARMACOLOGY,59(6),542-550.
MLA Zeng, Ke-Wu,et al."Icariin attenuates beta-amyloid-induced neurotoxicity by inhibition of tau protein hyperphosphorylation in PC12 cells".NEUROPHARMACOLOGY 59.6(2010):542-550.
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