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Curcumin attenuates the kainic acid-induced hippocampal cell death in the mice

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dc.contributor.authorShin, Hyun Joo-
dc.contributor.authorLee, Ji Yeong-
dc.contributor.authorSon, Eunyung-
dc.contributor.authorLee, Dong Hun-
dc.contributor.authorKim, Hyun Joon-
dc.contributor.authorKang, Sang Soo-
dc.contributor.authorCho, Gyeong Jae-
dc.contributor.authorChoi, Wan Sung-
dc.contributor.authorRoh, Gu Seob-
dc.date.accessioned2022-12-27T06:56:31Z-
dc.date.available2022-12-27T06:56:31Z-
dc.date.issued2007-04-
dc.identifier.issn0304-3940-
dc.identifier.issn1872-7972-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/28396-
dc.description.abstractKainic acid (KA) induced oxidative stress is associated with hippocampal cell death. Recent studies suggest that curcumin, a potent antioxidant, may provide protection for KA-induced oxidative stress. We investigated the effects of curcumin treatment on hippocampal reactive astrocytes in mice with KA-induced seizures. Eighteen hours after curcumin treatment, mice were treated with KA (30 mg/kg, i.p.), and then sacrificed after a further 48 h. Using cresyl violet staining and TUNEL analysis, histological evaluation revealed cell death in the KA-treated hippocampus. However, marked cell death was not observed in mice treated with curcumin. In addition, curcumin treatment reduced the KA-induced immunoreactivity of caspase-3. Similarly, immunoreactivity analyses indicated that KA causes upregulation of hippocampal GFAP, eNOS, and HO-1 levels, all of which were reduced in animals those received the curcumin treatment. Our findings indicate that curcumin is a potent inhibitor of reactive astrocyte expression and thus, prevents hippocampal cell death. These results also support its potential for use in the treatment of neurodegenerative diseases. (c) 2007 Elsevier Ireland Ltd. All rights reserved.-
dc.format.extent6-
dc.language영어-
dc.language.isoENG-
dc.publisherElsevier BV-
dc.titleCurcumin attenuates the kainic acid-induced hippocampal cell death in the mice-
dc.typeArticle-
dc.publisher.location아일랜드-
dc.identifier.doi10.1016/j.neulet.2007.01.060-
dc.identifier.scopusid2-s2.0-33947319691-
dc.identifier.wosid000246038900010-
dc.identifier.bibliographicCitationNeuroscience Letters, v.416, no.1, pp 49 - 54-
dc.citation.titleNeuroscience Letters-
dc.citation.volume416-
dc.citation.number1-
dc.citation.startPage49-
dc.citation.endPage54-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.subject.keywordPlusNITRIC-OXIDE SYNTHASE-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusEXCITOTOXIC INJURY-
dc.subject.keywordPlusBRAIN-
dc.subject.keywordPlusASTROCYTES-
dc.subject.keywordPlusNEURONS-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusINDUCTION-
dc.subject.keywordPlusGLUTAMATE-
dc.subject.keywordPlusISCHEMIA-
dc.subject.keywordAuthorastrocyte-
dc.subject.keywordAuthorcurcumin-
dc.subject.keywordAuthorhippocampus-
dc.subject.keywordAuthorkainic acid-
dc.subject.keywordAuthormice-
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