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Neuroprotective Effect of Membrane-Free Stem Cell Extract against Amyloid Beta (25-35)-Induced Neurotoxicity in SH-SY5Y Cells

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dc.contributor.authorPark, Hye Sook-
dc.contributor.authorPang, Qi Qi-
dc.contributor.authorKim, Young Sil-
dc.contributor.authorKim, Ji Hyun-
dc.contributor.authorCho, Eun Ju-
dc.date.accessioned2022-12-26T10:31:21Z-
dc.date.available2022-12-26T10:31:21Z-
dc.date.issued2021-03-
dc.identifier.issn2076-3417-
dc.identifier.issn2076-3417-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/3992-
dc.description.abstractAmyloid beta (A beta) produced by the amyloidogenic pathway induces neurotoxicity, and its accumulation is a well-known cause of Alzheimer's disease (AD). In this study, the protective effect of membrane-free stem cell extract (MFSCE) derived from adipose tissue against A beta(25-35)-induced neurotoxicity in the neuronal cells was investigated. Treatment with MFSCE increased cell viability and decreased lactate dehydrogenase (LDH) release in a dose-dependent manner, compared with the A beta(25-35)-induced group. The level of reactive oxygen species (ROS) was significantly increased in neuronal cells induced by A beta(25-35), whereas MFSCE treatment dose-dependently reduced ROS production. Treatment with MFSCE attenuated neuroinflammation and neuronal apoptosis by downregulating inducible nitric oxide synthase, cyclooxygenase-2, and B-cell lymphoma 2-associated X protein in treated SH-SY5Y cells induced by A beta(25-35). Furthermore, MFSCE significantly downregulated the expression of the amyloidogenic pathway-related proteins, such as amyloid precursor protein, beta-secretase, preselin-1, and preselin-2. Therefore, this study indicated a neuroprotective effect of MFSCE against neurotoxicity induced by A beta(25-35), suggesting that it is a useful strategy for the treatment of AD.-
dc.format.extent12-
dc.language영어-
dc.language.isoENG-
dc.publisherMDPI-
dc.titleNeuroprotective Effect of Membrane-Free Stem Cell Extract against Amyloid Beta (25-35)-Induced Neurotoxicity in SH-SY5Y Cells-
dc.typeArticle-
dc.publisher.location스위스-
dc.identifier.doi10.3390/app11052219-
dc.identifier.scopusid2-s2.0-85102596881-
dc.identifier.wosid000627965100001-
dc.identifier.bibliographicCitationAPPLIED SCIENCES-BASEL, v.11, no.5, pp 1 - 12-
dc.citation.titleAPPLIED SCIENCES-BASEL-
dc.citation.volume11-
dc.citation.number5-
dc.citation.startPage1-
dc.citation.endPage12-
dc.type.docTypeArticle-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaChemistry-
dc.relation.journalResearchAreaEngineering-
dc.relation.journalResearchAreaMaterials Science-
dc.relation.journalResearchAreaPhysics-
dc.relation.journalWebOfScienceCategoryChemistry, Multidisciplinary-
dc.relation.journalWebOfScienceCategoryEngineering, Multidisciplinary-
dc.relation.journalWebOfScienceCategoryMaterials Science, Multidisciplinary-
dc.relation.journalWebOfScienceCategoryPhysics, Applied-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusALZHEIMERS-DISEASE-
dc.subject.keywordPlusCONDITIONED MEDIUM-
dc.subject.keywordPlusMEMORY DEFICITS-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusTRANSPLANTATION-
dc.subject.keywordPlusPEPTIDE-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusNEUROINFLAMMATION-
dc.subject.keywordPlusPROTECTION-
dc.subject.keywordAuthormembrane-free stem cell extract-
dc.subject.keywordAuthorneuroinflammation-
dc.subject.keywordAuthorAlzheimer&#8217-
dc.subject.keywordAuthors disease-
dc.subject.keywordAuthorreactive oxygen species-
dc.subject.keywordAuthoramyloid beta-
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