Abstract
Recent studies have shown that Korean Red Ginseng (KRG) suppresses dopaminergic neuronal death in the brain of a Parkinson’s disease (PD) mouse model, but the mechanism is still elusive. Using a 2-dimensional electrophoresis technique, we investigated whether KRG can restore the changes in protein expressions in the striatum (ST) of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-injected mice. Male C57BL/6 mice (9 weeks old) were injected with 20 mg/kg MPTP intraperitoneally four times at 2-h intervals. KRG (100 mg/kg) was orally administered once a day for 3 days from one hour after the first MPTP injection. Two hours after the third KRG administration a pole test was performed to evaluate motor function, after which the brains were immediately harvested. Survival of dopaminergic neurons in the nigrostriatal pathway and protein expression in the ST were measured by immunohistochemistry and 2-dimensional electrophoresis. KRG suppressed MPTP-induced behavioral dysfunction and neuronal death in the nigrostriatal pathway. Moreover, 30 proteins changed by MPTP and KRG in the ST were identified and shown to be related to glycolysis/gluconeogenesis and neurodegenerative diseases including Alzheimer’s disease and PD. KRG has neuroprotective effects against MPTP toxicity and alleviates protein expression profiles related to enhancing energy metabolism in the ST of MPTP-treated mice.
Highlights
Parkinson’s disease (PD) is a well-known neurodegenerative disease characterized by selective dopaminergic cell death in the substantia nigra (SN) and striatum (ST) [1]
This study demonstrated that Korean Red Ginseng (KRG) extract suppressed MPTP-induced dopaminergic neuronal death in the nigrostriatal pathway and restored the MPTP-induced proteomic changes in the ST
MPTP administration suppressed the motor function and expression of five proteins related to glycolysis and gluconeogenesis and three proteins related to oxidative phosphorylation, but their suppression was alleviated by KRG oral administration
Summary
Parkinson’s disease (PD) is a well-known neurodegenerative disease characterized by selective dopaminergic cell death in the substantia nigra (SN) and striatum (ST) [1]. Degeneration of the nigrostriatal pathway causes striatal dopamine deficiency, which leads to symptoms of PD [2]. The motor symptoms of PD are mainly due to dopaminergic neuronal degeneration in the SN. Recent studies have shown that PD develops cognitive impairments, which is related to the neuronal death in the ST [3].
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