RETRACTED ARTICLE: Fuzhisan, a Chinese Herbal Medicine, Inhibits Beta-Amyloid-Induced Neurotoxicity and Tau Phosphorylation Through Calpain/Cdk5 Pathway in Cultured Cortical Neurons

被引：8

作者：

Zhaoxu Zhang

Ruiping Zhao

Ying Tang

Shirong Wen

Desheng Wang

Jiping Qi

机构：

[1] the First Affiliated Hospital,Department of Neurology

[2] Harbin Medical University,Department of Pathology

[3] The First Affiliated Hospital,undefined

[4] Harbin Medical University,undefined

来源：

Neurochemical Research | 2011年 / 36卷

关键词：

Fuzhisan (FZS); Alzheimer’s disease; Tau; Cyclin-dependent kinase 5 (CDK5); p35; p25;

D O I：

暂无

中图分类号：

学科分类号：

摘要：

It has been shown that β-amyloid (Aβ) induced hyperphosphorylation of tau is implicated in the pathogenesis of Alzheimer’s disease (AD), and deregulation of cyclin-dependent kinase 5 (Cdk5) activity is involved in the abnormal tau phosphorylation. The cleavage of neuron-specific Cdk5 activator, p35, to p25, mediated by calpain and calcium, deregulates Cdk5 activity and promotes neurodegeneration. Fuzhisan (FZS), a Chinese herbal complex prescription that has been used for the treatment of AD for over 15 years, is known to enhance the cognitive ability in AD patients. In this study, we investigated the neuroprotective effects and potential molecular mechanisms of FZS against Aβ25–35-induced toxicity in cultured cortical neurons. We revealed that FZS attenuated Aβ25–35-induced neurotoxicity in a dose-dependent manner. FZS inhibited Aβ25–35-induced activation of Cdk5 and decreased tau hyperphosphorylation although it did not directly inhibit Cdk5. In addition, FZS also blocked Aβ25–35-induced calcium influx, calpain activation and decreased cleavage of p35 to p25.

引用

页码：801 / 811

页数：10

共 109 条

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