Neuroprotective effects of astragaloside IV on Parkinson disease models of mice and primary astrocytes
- Lei Xia
- Dianxuan Guo
- Bing Chen
Published online on: September 29, 2017
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.