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Cited 6 time in webofscience Cited 7 time in scopus
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Cilostazol attenuates kainic acid-induced hippocampal cell death

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dc.contributor.authorPark, Young-Seop-
dc.contributor.authorJin, Zhen-
dc.contributor.authorJeong, Eun Ae-
dc.contributor.authorYi, Chin-ok-
dc.contributor.authorLee, Jong Youl-
dc.contributor.authorPark, In Sung-
dc.contributor.authorRoh, Gu Seob-
dc.date.accessioned2022-12-26T17:18:13Z-
dc.date.available2022-12-26T17:18:13Z-
dc.date.issued2018-01-
dc.identifier.issn1226-4512-
dc.identifier.issn2093-3827-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/12030-
dc.description.abstractCilostazol is a selective inhibitor of type 3 phosphodiesterase (PDE3) and has been widely used as an antiplatelet agent. Cilostazol mediates this activity through effects on the cyclic adenosine monophosphate (cAMP) signaling cascade. Recently, it has attracted attention as a neuroprotective agent. However, little is known about cilostazol's effect on excitotoxicity induced neuronal cell death. Therefore, this study evaluated the neuroprotective effect of cilostazol treatment against hippocampal neuronal damage in a mouse model of kainic acid (KA)-induced neuronal loss. Cilostazol pretreatment reduced KA-induced seizure scores and hippocampal neuron death. In addition, cilostazol pretreatment increased cAMP response element-binding protein (CREB) phosphorylation and decreased neuroinflammation. These observations suggest that cilostazol may have beneficial therapeutic effects on seizure activity and other neurological diseases associated with excitotoxicity.-
dc.format.extent8-
dc.language영어-
dc.language.isoENG-
dc.publisher대한약리학회-
dc.titleCilostazol attenuates kainic acid-induced hippocampal cell death-
dc.typeArticle-
dc.publisher.location대한민국-
dc.identifier.doi10.4196/kjpp.2018.22.1.63-
dc.identifier.scopusid2-s2.0-85041180062-
dc.identifier.wosid000422818400007-
dc.identifier.bibliographicCitationThe Korean Journal of Physiology & Pharmacology, v.22, no.1, pp 63 - 70-
dc.citation.titleThe Korean Journal of Physiology & Pharmacology-
dc.citation.volume22-
dc.citation.number1-
dc.citation.startPage63-
dc.citation.endPage70-
dc.type.docTypeArticle-
dc.identifier.kciidART002308360-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalResearchAreaPhysiology-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryPhysiology-
dc.subject.keywordPlusELEMENT-BINDING PROTEIN-
dc.subject.keywordPlusCHRONIC CEREBRAL HYPOPERFUSION-
dc.subject.keywordPlusKAINATE-INDUCED EXCITOTOXICITY-
dc.subject.keywordPlusRAT HIPPOCAMPUS-
dc.subject.keywordPlusPHOSPHODIESTERASE TYPE-3-
dc.subject.keywordPlusMICROGLIAL ACTIVATION-
dc.subject.keywordPlusMOUSE HIPPOCAMPUS-
dc.subject.keywordPlusINJURY-
dc.subject.keywordPlusBRAIN-
dc.subject.keywordPlusINHIBITOR-
dc.subject.keywordAuthorCilostazol-
dc.subject.keywordAuthorHippocampus-
dc.subject.keywordAuthorKainic acid-
dc.subject.keywordAuthorNeuroinflammation-
dc.subject.keywordAuthorNeuronal death-
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