Panax ginseng is neuroprotective in a novel progressive model of Parkinson's disease.
Identifieur interne : 001640 ( Ncbi/Checkpoint ); précédent : 001639; suivant : 001641Panax ginseng is neuroprotective in a novel progressive model of Parkinson's disease.
Auteurs : Jackalina M. Van Kampen [Canada] ; David B. Baranowski [Canada] ; Christopher A. Shaw [Canada] ; Denis G. KaySource :
- Experimental gerontology [ 1873-6815 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Cell Death (drug effects), Disease Models, Animal, Disease Progression, Drug Evaluation, Preclinical (methods), Encephalitis (chemically induced), Encephalitis (prevention & control), Female, Gait Disorders, Neurologic (chemically induced), Gait Disorders, Neurologic (prevention & control), Neuroprotective Agents (therapeutic use), Panax, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (metabolism), Parkinson Disease, Secondary (pathology), Parkinson Disease, Secondary (prevention & control), Phytotherapy (methods), Plant Extracts (therapeutic use), Rats, Rats, Sprague-Dawley, Sitosterols, Substantia Nigra (pathology), alpha-Synuclein (metabolism).
- MESH :
- chemical , metabolism : alpha-Synuclein.
- chemical , therapeutic use : Neuroprotective Agents, Plant Extracts.
- chemically induced : Encephalitis, Gait Disorders, Neurologic, Parkinson Disease, Secondary.
- drug effects : Cell Death.
- metabolism : Parkinson Disease, Secondary.
- methods : Drug Evaluation, Preclinical, Phytotherapy.
- pathology : Parkinson Disease, Secondary, Substantia Nigra.
- prevention & control : Encephalitis, Gait Disorders, Neurologic, Parkinson Disease, Secondary.
- Animals, Disease Models, Animal, Disease Progression, Female, Panax, Rats, Rats, Sprague-Dawley, Sitosterols.
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.
DOI: 10.1016/j.exger.2013.11.012
PubMed: 24316034
Affiliations:
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Electronic address: jvankampen@neurodyn.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>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</wicri:regionArea><wicri:noRegion>PE C1A 4P3</wicri:noRegion></affiliation></author><author><name sortKey="Baranowski, David B" sort="Baranowski, David B" uniqKey="Baranowski D" first="David B" last="Baranowski">David B. 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Van Kampen</name><affiliation wicri:level="1"><nlm:affiliation>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.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>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</wicri:regionArea><wicri:noRegion>PE C1A 4P3</wicri:noRegion></affiliation></author><author><name sortKey="Baranowski, David B" sort="Baranowski, David B" uniqKey="Baranowski D" first="David B" last="Baranowski">David B. 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Shaw</name><affiliation wicri:level="1"><nlm:affiliation>Department of Ophthalmology and Visual Sciences, University of British Columbia, 828W. 10th Ave., Vancouver, BC V5Z 1L8, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Ophthalmology and Visual Sciences, University of British Columbia, 828W. 10th Ave., Vancouver, BC V5Z 1L8</wicri:regionArea><wicri:noRegion>BC V5Z 1L8</wicri:noRegion></affiliation></author><author><name sortKey="Kay, Denis G" sort="Kay, Denis G" uniqKey="Kay D" first="Denis G" last="Kay">Denis G. Kay</name><affiliation><nlm:affiliation>Neurodyn Inc., 550 University Ave., Charlottetown, PE C1A 4P3, Canada; Department of Biochemistry, University of Prince Edward Island.</nlm:affiliation><wicri:noCountry code="subField">University of Prince Edward Island</wicri:noCountry></affiliation></author></analytic><series><title level="j">Experimental gerontology</title><idno type="eISSN">1873-6815</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Death (drug effects)</term><term>Disease Models, Animal</term><term>Disease Progression</term><term>Drug Evaluation, Preclinical (methods)</term><term>Encephalitis (chemically induced)</term><term>Encephalitis (prevention & control)</term><term>Female</term><term>Gait Disorders, Neurologic (chemically induced)</term><term>Gait Disorders, Neurologic (prevention & control)</term><term>Neuroprotective Agents (therapeutic use)</term><term>Panax</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (metabolism)</term><term>Parkinson Disease, Secondary (pathology)</term><term>Parkinson Disease, Secondary (prevention & control)</term><term>Phytotherapy (methods)</term><term>Plant Extracts (therapeutic use)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Sitosterols</term><term>Substantia Nigra (pathology)</term><term>alpha-Synuclein (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Neuroprotective Agents</term><term>Plant Extracts</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Encephalitis</term><term>Gait Disorders, Neurologic</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Death</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Drug Evaluation, Preclinical</term><term>Phytotherapy</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease, Secondary</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Encephalitis</term><term>Gait Disorders, Neurologic</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Disease Progression</term><term>Female</term><term>Panax</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Sitosterols</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Kay, Denis G" sort="Kay, Denis G" uniqKey="Kay D" first="Denis G" last="Kay">Denis G. Kay</name></noCountry><country name="Canada"><noRegion><name sortKey="Van Kampen, Jackalina M" sort="Van Kampen, Jackalina M" uniqKey="Van Kampen J" first="Jackalina M" last="Van Kampen">Jackalina M. Van Kampen</name></noRegion><name sortKey="Baranowski, David B" sort="Baranowski, David B" uniqKey="Baranowski D" first="David B" last="Baranowski">David B. Baranowski</name><name sortKey="Shaw, Christopher A" sort="Shaw, Christopher A" uniqKey="Shaw C" first="Christopher A" last="Shaw">Christopher A. Shaw</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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