Panax ginseng has been used in traditional Chinese medicine for centuries. Among its various benefits is a pluripotent targeting of the various events involved in neuronal cell death. This includes anti-inflammatory, anti-oxidant, and anti-apoptotic effects. Indeed, ginseng extract and its individual ginsenosides have been demonstrated to influence a number of biochemical markers implicated in Parkinson's disease (PD) pathogenesis. We have reported previously that administration of the ginseng extract, G115, afforded robust neuroprotection in two rodent models of PD. However, these traditional rodent models are acute in nature and do accurately recapitulate the progressive nature of the disease. Chronic exposure to the dietary phytosterol glucoside, β-sitosterol β-d-glucoside (BSSG) triggers the progressive development of neurological deficits, with behavioral and cellular features that closely approximate those observed in PD patients. Clinical signs and histopathology continue to develop for several months following cessation of exposure to the neurotoxic insult. Here, we utilized this model to further characterize the neuroprotective effects of the ginseng extract, G115. Oral administration of this extract significantly reduced dopaminergic cell loss, microgliosis, and accumulation of α-synuclein aggregates. Further, G115 administration fully prevented the development of locomotor deficits, in the form of reduced locomotor activity and coordination. These results suggest that ginseng extract may be a potential neuroprotective therapy for the treatment of PD.
Keywords: BSSG; DAT; Dopamine; ER; G115; GRP; Ginseng; Neuroprotection; PD; Parkinson's disease; SNc; Substantia nigra; TH; TUNEL; UPR; dopamine transporter; endoplasmic reticulum; glucose-regulated protein; substantia nigra pars compacta; terminal deoxynucleotidyl transferase dUTP nick end labeling; tyrosine hydroxylase; unfolded protein response; α-Synuclein; β-sitosterol β-d-glucoside.
Copyright © 2013 Elsevier Inc. All rights reserved.