Involvement of calpain and p25 of CDK5 pathway in ginsenoside Rb1's attenuation of β-amyloid peptide_25–35-induced tau hyperphosphorylation in cortical neurons

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• 作者：Xiaochun Chen ; Tianwen Huang ; Jing Zhang ; Jinqiu Song ; Limin Chen ; Yuangui Zhu
• 关键词：Ginsenoside Rb1 ; β ; -amyloid (Aβ ; ) ; Tau ; Cyclin-dependent kinase 5 (CDK5) ; p35 ; p25
• 刊名：Brain Research
• 出版年：2008
• 出版时间：20 March 2008
• 年：2008
• 卷：1200
• 期：Complete
• 页码：99-106
• 全文大小：425 K

文摘

Increasing evidence have shown that β-amyloid (Aβ) induced hyperphosphorylation of tau, which eventually resulted in the disruption of microtubule (MT) integrity. Cyclin-dependent kinase 5 (CDK5) and its activator p35 are required for neurite outgrowth. The cleavage of p35 to p25, mediated by calpain and calcium, caused CDK5 dislocation and subsequently p25/CDK5-induced tau hyperphosphorylation, which disrupted the cytoskeleton and resulted in neuronal death. In the present study we investigated the effects of ginsenoside Rb1 on fibrillar Aβ_25–35-induced tau hyperphosphorylation in primary cultured cortical neurons and also the potential involvement of Ca²⁺-calpain-CDK5 signal pathway. The present study suggests that Ca²⁺, calpain, and p25 in CDK5 pathway may play important roles in Aβ_25–35-induced tau hyperphosphorylation.