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Neuroprotective effects of extract of Acanthopanax senticosus harms on WT-α-Syn or A53T-α-Syn transgenic SH-SY5Y cells
LI Xuzhao 1 #,WANG Kexin 1,ZHANG Shuainan 1,YANG Zhiming 1,LIU Hong-yu 2,LU Fang 1,Liu Shumin 3 *
1.Chinese Medicine Toxicological Laboratory, Institute of Traditional Chinese Medicine, Heilongjiang University of Chinese Medicine, Harbin 150040
2.First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing 210046
3.Drug Safety Evaluation Center, Heilongjiang University of Chinese Medicine, Harbin 150040
*Correspondence author
#Submitted by
Subject:
Funding: the National Natural Science Foundation of China（No.81073019）, This article is supported by the Specialized Research Fund for the Doctoral Program of Higher Education of China （No.20102327110004）
Opened online: 5 August 2013
Accepted by: none
Citation: LI Xuzhao,WANG Kexin,ZHANG Shuainan.Neuroprotective effects of extract of Acanthopanax senticosus harms on WT-α-Syn or A53T-α-Syn transgenic SH-SY5Y cells[OL]. [ 5 August 2013] http://en.paper.edu.cn/en_releasepaper/content/4553526
 
 
AIM: Extract of Acanthopanax senticosus harms (EAS) has been shown to have neuroprotective effects on dopaminergic neurons in Parkinson's disease (PD) mice model. α-Synuclein is a key player in the pathogenesis of PD, the elevated level of which is deleterious to dopaminergic neurons, and enhancing its clearance might be a promising strategy for treating PD. To assess the potential of EAS in this regard, we investigated its effect on the SH-SY5Y cells overexpressing wild-type α-synuclein (WT-α-Syn) or A53T mutant α-synuclein (A53T-α-Syn) and the implicated pathway it might mediate. METHODS: After treatment with EAS, the effect of EAS on apoptosis in these two transgenic cells was analyzed by flow cytometry. The changes of α-synuclein, caspase-3, parkin, phospho-protein kinase B (Akt), phospho-glycogen synthase kinase 3 beta (GSK3β), and phospho-microtubule-associated protein tau (Tau) in WT-α-Syn or A53T-α-Syn transgenic cells were analyzed by western blotting and quantitative real-time PCR. RESULTS: The changes of α-synuclein, caspase-3, parkin, phospho-Akt, phospho-GSK3β, and phospho-Tau in WT-α-Syn or A53T-α-Syn transgenic cells were reverted back to near normal levels. CONCLUSION: The neuroprotective effects of EAS may be able to protect WT-α-Syn or A53T-α-Syn transgenic SH-SY5Y cells from α-synuclein overexpression and toxicity. Therefore, we speculate that EAS might be a promising candidate for prevention or treatment of α-synuclein-related neurodegenerative disorders such as PD.
Keywords:Traditional Chinese Medicine; Acanthopanax senticosus harms; Parkinson's disease; α-synuclein
 
 
 

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