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Citicoline reduces upregulated clusterin following kainic acid injection in the rat retina

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dc.contributor.authorPark, Chang Hwan-
dc.contributor.authorKim, Yoon Sook-
dc.contributor.authorLee, Ho Kyung-
dc.contributor.authorKim, Young Hee-
dc.contributor.authorChoi, Mee Young-
dc.contributor.authorJung, Dhong Eun-
dc.contributor.authorYoo, Ji Myong-
dc.contributor.authorKang, Sang Soo-
dc.contributor.authorChoi, Wan Sung-
dc.contributor.authorCho, Gyeong Jae-
dc.date.accessioned2022-12-27T06:51:05Z-
dc.date.available2022-12-27T06:51:05Z-
dc.date.issued2007-12-
dc.identifier.issn0271-3683-
dc.identifier.issn1460-2202-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/28230-
dc.description.abstractPurpose: To investigate the effects of citicoline on upregulated clusterin and retinal damage induced by kainic acid (KA). Methods: KA was injected into the vitreous of rats. Effects of systemic citicoline treatments were estimated by measuring the thickness of the various retinal layers, immunoblotting, and immunohistochemical techniques. Results: One day after KA injection, the immunoreactivity of clusterin increased significantly. In rats treated with KA plus clusterin immunoreactivity was markedly reduced compared to KA-treated rats. Western blot analysis showed that clusterin protein levels were increased in KA-treated rats, but decreased in KA plus citicoline-treated rats. Apoptotic cell death was determined by TUNEL method. Citicoline reduced the expression of clusterin, as well as the expression of TUNEL after KA injection in the rat retina. Conclusion: The increased expression of clusterin following KA injection in the rat retina suggests the presence of neurodegenerative events; citicoline may provide neuroprotection against neuronal cell damage.-
dc.format.extent9-
dc.language영어-
dc.language.isoENG-
dc.publisherTAYLOR & FRANCIS INC-
dc.titleCiticoline reduces upregulated clusterin following kainic acid injection in the rat retina-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1080/02713680701758719-
dc.identifier.scopusid2-s2.0-39149098465-
dc.identifier.wosid000252090300007-
dc.identifier.bibliographicCitationCURRENT EYE RESEARCH, v.32, no.12, pp 1055 - 1063-
dc.citation.titleCURRENT EYE RESEARCH-
dc.citation.volume32-
dc.citation.number12-
dc.citation.startPage1055-
dc.citation.endPage1063-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOphthalmology-
dc.relation.journalWebOfScienceCategoryOphthalmology-
dc.subject.keywordPlusTRANSIENT CEREBRAL-ISCHEMIA-
dc.subject.keywordPlusCDP-CHOLINE-
dc.subject.keywordPlusCELL-DEATH-
dc.subject.keywordPlusSULFATED GLYCOPROTEIN-2-
dc.subject.keywordPlusINTRAOCULAR INJECTION-
dc.subject.keywordPlusCASPASE-3 ACTIVATION-
dc.subject.keywordPlusALZHEIMERS-DISEASE-
dc.subject.keywordPlusPHOSPHOLIPASE A(2)-
dc.subject.keywordPlusGLUTAMATE LEVELS-
dc.subject.keywordPlusGENE-EXPRESSION-
dc.subject.keywordAuthorciticoline-
dc.subject.keywordAuthorclusterin-
dc.subject.keywordAuthorkainic acid-
dc.subject.keywordAuthorrat-
dc.subject.keywordAuthorretina-
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