title: Panax ginseng is neuroprotective in a novel progressive model of Parkinson's disease.
abstract: 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.
authors: Neurodyn Inc., 550 University Ave., Charlottetown, PE C1A 4P3, Canada; Department of Biomedical Science, University of Prince Edward Island, 550 University Ave., Charlottetown, PE C1A 4P3, Canada. Electronic address: jvankampen@neurodyn.ca.
authors: Jackalina M
authors: JM
authors: Van Kampen
authors: Neurodyn Inc., 550 University Ave., Charlottetown, PE C1A 4P3, Canada.
authors: David B
authors: DB
authors: Baranowski
authors: Department of Ophthalmology and Visual Sciences, University of British Columbia, 828W. 10th Ave., Vancouver, BC V5Z 1L8, Canada.
authors: Christopher A
authors: CA
authors: Shaw
authors: Neurodyn Inc., 550 University Ave., Charlottetown, PE C1A 4P3, Canada; Department of Biochemistry, University of Prince Edward Island.
authors: Denis G
authors: DG
authors: Kay
mesh_terms: D000818:Animals; D016923:Cell Death / Q000187:drug effects; D004195:Disease Models, Animal; D018450:Disease Progression; D004353:Drug Evaluation, Preclinical / Q000379:methods; D004660:Encephalitis / Q000139:chemically induced / Q000517:prevention & control; D005260:Female; D020233:Gait Disorders, Neurologic / Q000139:chemically induced / Q000517:prevention & control; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D005894:Panax; D010302:Parkinson Disease, Secondary / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D008517:Phytotherapy / Q000379:methods*; D010936:Plant Extracts / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D012855:Sitosterols; D013378:Substantia Nigra / Q000473:pathology; D051844:alpha-Synuclein / Q000378:metabolism
chemical_list: D018696:Neuroprotective Agents; D010936:Plant Extracts; D012855:Sitosterols; D051844:alpha-Synuclein; C011015:lyoniside
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