Neuroprotective effects of astragaloside IV on Parkinson disease models of mice and primary astrocytes

Parkinson's disease (PD) is characterized by a progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta. Inflammation and neural degeneration are implicated in the pathogenesis of PD. Astragaloside IV (AS-IV) has been verified to attenuate inflammation. The current...

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Bibliographic Details
Published in:Experimental and therapeutic medicine 2017-12, Vol.14 (6), p.5569-5575
Main Authors: Xia, Lei, Guo, Dianxuan, Chen, Bing
Format: Article
Language:English
Subjects:
Alzheimer's disease
Analysis
astragaloside IV
astrocytes
Care and treatment
Chinese herbal medicine
Ethanol
Health aspects
Inflammation
Laboratory animals
Neuroprotective agents
Parkinson disease
Parkinson's disease
Physiological aspects
Studies
Swimming
Traumatic brain injury
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Summary:Parkinson's disease (PD) is characterized by a progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta. Inflammation and neural degeneration are implicated in the pathogenesis of PD. Astragaloside IV (AS-IV) has been verified to attenuate inflammation. The current study aimed to investigate the role of AS-IV in PD and the possible molecular mechanisms. Pole, traction and swim tests were performed to examine the effects of AS-IV on 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-generated behavioral deficiencies in vivo. Meanwhile, as for in vitro experiments, the influence of AS-IV on cell viability was evaluated using the 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay, the effects of AS-IV on 1-methyl-4-phenylpyridnium ion (MPP+)-induced cell viability changes were tested using MTT assays, cell apoptosis rates were assessed using an Annexin-V Fluorescein isothiocyanate kit, and the expression levels of phosphorylated-Jun N-terminal kinase (p-JNK), Bcl-2-associated X protein (Bax)/Bcl-2 and caspase-3 activity were assessed using western blot analysis. Behavioral tests showed that pretreatment of AS-IV significantly alleviated MPTP-generated behavioral deficiencies in vivo. Meanwhile, AS-IV remarkably rescued MPP+-induced cell viability reduction, increase in cell apoptosis rate, and upregulation of p-JNK, Bax/Bcl-2 ratio and caspase-3 activity in vitro. In conclusion, AS-IV may be a promising neuroprotective agent for PD.
ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2017.5238