Abstract
The present study aimed to investigate the protective effect of compound formula Rehmannia (CFR) against the development of Parkinson's disease (PD). After the in vivo and in vitro models of PD were established with overexpression α-syn induced, CFR was administrated into the PD model rats for 6 weeks or SK-N-SH cells with coincubation for 48 h. Apomorphine-induced rotation test, CCK8 assay, TUNEL assay, immunofluorescence staining, and western blot assay were performed to evaluate the behavioral changes, cell viability, cell apoptosis, α-syn, GSK-3β, P-GSK-3β (Ser9), P-GSK-3β (Tyr216), and β-catenin expression in PD rats or SK-N-SH cells. PD rat behavior results showed that the rotation numbers were significantly decreased in the CFR treatment group comparing with the AAV-α-syn PD model group. The cell viability suppressed by H2O2 and α-syn in SK-N-SH model cells was also significantly improved with CFR administration. Cell apoptosis and α-syn overexpression observed in PD rats and SK-N-SH cells were also inhibited by CFR treatment. Furthermore, the protein expression of α-syn, GSK-3β, P-GSK-3β (Ser9), P-GSK-3β (Tyr216), and β-catenin in in vivo and in vitro was also significantly regulated by CFR. The present study suggested that CFR may be considered as a potential neuroprotective agent against PD, and this application will require further investigation.
Highlights
Parkinson’s disease (PD) is a common neurodegenerative disease prevalent in middle-aged and elderly populations
TUNEL-positive cells in the PD model group were significantly increased compared with the control group, inducing the cellular apoptosis (P < 0.01)
TUNEL-positive cells in the PD model group were obviously increased compared with the control group, and the compound formula Rehmannia (CFR) treatment for the PD rat model decreased the TUNEL-positive cells compared with the model group (P < 0.01)
Summary
Parkinson’s disease (PD) is a common neurodegenerative disease prevalent in middle-aged and elderly populations. E epidemiological studies report that the prevalence of PD is about 0.3%, while the incidence is doubled with the incidence of 1% to 2% in the elders over 65 years old and 3% to 5% in the elders over 85 years old [2]. PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and loss of dopamine (DA) in the striatum [3]. Oxidative stress and mitochondrial dysfunction are involved in the degeneration and loss of dopaminergic neurons in the substantia nigra. Talking of the side effects, the most seriuos one is the L-Dopa-induced dyskinesia, the clinical manifestation mainly resembles dance, which seriously affects the quality of daily life of PD patients and creates an escalating burden on the family and society [4]
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