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Article: Neuroprotective effects of ginsenoside-Rg1 in primary nigral neurons against rotenone toxicity

TitleNeuroprotective effects of ginsenoside-Rg1 in primary nigral neurons against rotenone toxicity
Authors
KeywordsApoptosis
Ginsenoside-Rg1
Neurodegenerative diseases
Neuroprotection
Rotenone
Substantia nigra
Issue Date2007
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neuropharm
Citation
Neuropharmacology, 2007, v. 52 n. 3, p. 827-835 How to Cite?
AbstractGinsenoside-Rg1, the pharmacologically active component isolated from ginseng, demonstrated neuroprotective effects on primary cultured rat nigral neurons against rotenone toxicity. Rotenone, a common household pesticide known for its specific and irreversible mitochondria complex I inhibition, has been suggested to be the causal agent of Parkinson's disease (PD) by inducing degeneration of cells in the substantial nigra. The present study demonstrated that co-treatment of rotenone and Rg1 could reduce rotenone-induced cell death by 58% (SEM = ±5.60; N = 3). Rotenone-induced mitochondria membrane potential (MMP, ΔΨm) depletion was restored and elevated by at least 38% (SEM = ±2.15; N = 3) by Rg1. In addition, Rg1 prevented cytochrome c release from the mitochrondrial membrane and increased the phosphorylation inhibition of the pro-apoptotic protein Bad through activation of the PI3K/Akt pathway. The protective effects of Rg1 was blocked by glucocorticoid receptor antagonist RU486, indicating that the action of Rg1 is mediated through glucocorticoid receptor (GR). In conclusion, Rg1 inhibits the mitochondrial apoptotic pathway and increases the survival chance of the primary cultured nigral neurons against rotenone toxicity. Thus, Rg1 and its related compounds may be developed as protective agents against neurodegenerative diseases induced by mitochondrial toxins. © 2006 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/81257
ISSN
2023 Impact Factor: 4.6
2023 SCImago Journal Rankings: 1.489
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, KWen_HK
dc.contributor.authorYung, KKLen_HK
dc.contributor.authorMak, NKen_HK
dc.contributor.authorChan, YSen_HK
dc.contributor.authorFan, TPen_HK
dc.contributor.authorWong, RNSen_HK
dc.date.accessioned2010-09-06T08:15:37Z-
dc.date.available2010-09-06T08:15:37Z-
dc.date.issued2007en_HK
dc.identifier.citationNeuropharmacology, 2007, v. 52 n. 3, p. 827-835en_HK
dc.identifier.issn0028-3908en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81257-
dc.description.abstractGinsenoside-Rg1, the pharmacologically active component isolated from ginseng, demonstrated neuroprotective effects on primary cultured rat nigral neurons against rotenone toxicity. Rotenone, a common household pesticide known for its specific and irreversible mitochondria complex I inhibition, has been suggested to be the causal agent of Parkinson's disease (PD) by inducing degeneration of cells in the substantial nigra. The present study demonstrated that co-treatment of rotenone and Rg1 could reduce rotenone-induced cell death by 58% (SEM = ±5.60; N = 3). Rotenone-induced mitochondria membrane potential (MMP, ΔΨm) depletion was restored and elevated by at least 38% (SEM = ±2.15; N = 3) by Rg1. In addition, Rg1 prevented cytochrome c release from the mitochrondrial membrane and increased the phosphorylation inhibition of the pro-apoptotic protein Bad through activation of the PI3K/Akt pathway. The protective effects of Rg1 was blocked by glucocorticoid receptor antagonist RU486, indicating that the action of Rg1 is mediated through glucocorticoid receptor (GR). In conclusion, Rg1 inhibits the mitochondrial apoptotic pathway and increases the survival chance of the primary cultured nigral neurons against rotenone toxicity. Thus, Rg1 and its related compounds may be developed as protective agents against neurodegenerative diseases induced by mitochondrial toxins. © 2006 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neuropharmen_HK
dc.relation.ispartofNeuropharmacologyen_HK
dc.subjectApoptosisen_HK
dc.subjectGinsenoside-Rg1en_HK
dc.subjectNeurodegenerative diseasesen_HK
dc.subjectNeuroprotectionen_HK
dc.subjectRotenoneen_HK
dc.subjectSubstantia nigraen_HK
dc.titleNeuroprotective effects of ginsenoside-Rg1 in primary nigral neurons against rotenone toxicityen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0028-3908&volume=52&spage=827&epage=835&date=2007&atitle=Neuroprotective+effects+of+Ginsenoside-Rg1+in+primary+nigral+neurons+against+rotenone+toxicityen_HK
dc.identifier.emailLeung, KW: kwleung1@hku.hken_HK
dc.identifier.emailChan, YS: yschan@hku.hken_HK
dc.identifier.authorityLeung, KW=rp01674en_HK
dc.identifier.authorityChan, YS=rp00318en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.neuropharm.2006.10.001en_HK
dc.identifier.pmid17123556-
dc.identifier.scopuseid_2-s2.0-33846890205en_HK
dc.identifier.hkuros137665en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33846890205&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume52en_HK
dc.identifier.issue3en_HK
dc.identifier.spage827en_HK
dc.identifier.epage835en_HK
dc.identifier.isiWOS:000244962600015-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLeung, KW=13106059300en_HK
dc.identifier.scopusauthoridYung, KKL=13605496000en_HK
dc.identifier.scopusauthoridMak, NK=35587830100en_HK
dc.identifier.scopusauthoridChan, YS=7403676627en_HK
dc.identifier.scopusauthoridFan, TP=7202528295en_HK
dc.identifier.scopusauthoridWong, RNS=7402126957en_HK
dc.identifier.issnl0028-3908-

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