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Chrysophanol Suppressed Glutamate-Induced Hippocampal Neuronal Cell Death via Regulation of Dynamin-Related Protein 1-Dependent Mitochondrial Fission

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dc.contributor.authorChae, Unbin-
dc.contributor.authorMin, Ju-Sik-
dc.contributor.authorLeem, Hyun Hee-
dc.contributor.authorLee, Hyun-Shik-
dc.contributor.authorLee, Hong Jun-
dc.contributor.authorLee, Sang-Rae-
dc.contributor.authorLee, Dong-Seok-
dc.date.accessioned2021-06-18T08:43:50Z-
dc.date.available2021-06-18T08:43:50Z-
dc.date.issued2017-08-01-
dc.identifier.issn0031-7012-
dc.identifier.issn1423-0313-
dc.identifier.urihttps://scholarworks.bwise.kr/cau/handle/2019.sw.cau/45647-
dc.description.abstractChrysophanic acid, or chrysophanol, is an anthraquinone found in Rheum palmatum, which was used in the preparation of oriental medicine in ancient China. The hippocampus plays a major role in controlling the activities of the short- and long-term memory. It is one of the major regions affected by excessive cell death in Alzheimer's disease. Therefore, neuronal cell-death modulation in the hippocampus is important for maintaining neuronal function. We investigated chrysophanol's effects on glutamate-induced hippocampal neuronal cell death. Chrysophanol reduced glutamate-induced cell death via suppression of proapoptotic factors and reactive oxygen species generation. Furthermore, it downregulated glutamate-induced mitochondrial fission by inhibiting dynamin-related protein 1 (Drp1) dephosphorylation. Thus, chrysophanol suppressed hippocampal neuronal cell death via inhibition of Drp1-dependent mitochondrial fission, and can be used as a therapeutic agent for treating neuronal cell death-mediated neurodegenerative diseases. (C) 2017 S. Karger AG, Basel-
dc.format.extent8-
dc.language영어-
dc.language.isoENG-
dc.publisherKARGER-
dc.titleChrysophanol Suppressed Glutamate-Induced Hippocampal Neuronal Cell Death via Regulation of Dynamin-Related Protein 1-Dependent Mitochondrial Fission-
dc.typeArticle-
dc.identifier.doi10.1159/000477814-
dc.identifier.bibliographicCitationPHARMACOLOGY, v.100, no.3-4, pp 153 - 160-
dc.description.isOpenAccessN-
dc.identifier.wosid000407176000007-
dc.identifier.scopusid2-s2.0-85021151963-
dc.citation.endPage160-
dc.citation.number3-4-
dc.citation.startPage153-
dc.citation.titlePHARMACOLOGY-
dc.citation.volume100-
dc.type.docTypeArticle-
dc.publisher.location스위스-
dc.subject.keywordAuthorChrysophanol-
dc.subject.keywordAuthorMitochondrial fission-
dc.subject.keywordAuthorDynamin-related protein 1-
dc.subject.keywordAuthorReactive oxygen species-
dc.subject.keywordAuthorNeuronal cell death-
dc.subject.keywordPlusNEURODEGENERATIVE DISEASES-
dc.subject.keywordPlusALZHEIMERS-DISEASE-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusPOWDERY MILDEW-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusDYSFUNCTION-
dc.subject.keywordPlusDISORDERS-
dc.subject.keywordPlusPHYSCION-
dc.subject.keywordPlusINSIGHTS-
dc.subject.keywordPlusNECROSIS-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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