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dc.contributor.author이영주-
dc.date.accessioned2019-11-30T18:28:07Z-
dc.date.available2019-11-30T18:28:07Z-
dc.date.issued2017-09-
dc.identifier.citationDementia and Neurocognitive Disorders(대한치매학회지), v. 16, no. 3, page. 64-71en_US
dc.identifier.isbn10.12779/dnd.2017.16.3.64-
dc.identifier.issn1738-1495-
dc.identifier.issn2384-0757-
dc.identifier.urihttps://synapse.koreamed.org/DOIx.php?id=10.12779/dnd.2017.16.3.64-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/115647-
dc.description.abstractBackground and Purpose Neurogenesis in the adult brain is important for memory and learning, and the alterations in neural stem cells (NSCs) may be an important aspect of Alzheimer’s disease (AD) pathogenesis. The phosphatidylinositol 3-kinase (PI3K) pathway has been suggested to have an important role in neuronal cell survival and is highly involved in adult neurogenesis. Candesartan is an angiotensin II receptor antagonist used for the treatment of hypertension and several studies have reported that it also has some neuroprotective effects. We investigated whether candesartan could restore the amyloid-β(25–35) (Aβ25-35) oligomer-inhibited proliferation of NSCs by focusing on the PI3K pathway. Methods To evaluate the effects of candesartan on the Aβ25-35 oligomer-inhibited proliferation of NSCs, the NSCs were treated with several concentrations of candesartan and/or Aβ25-35 oligomers, and MTT assay and trypan blue staining were performed. To evaluate the effect of candesartan on the Aβ-inhibited proliferation of NSCs, we performed a bromodeoxyuridine (BrdU) labeling assay. The levels of p85α PI3K, phosphorylated Akt (pAkt) (Ser473), phosphorylated glycogen sinthase kinase-3β (pGSK-3β) (Ser9), and heat shock transcription factor-1 (HSTF1) were analyzed by Western blotting. Results The BrdU assays demonstrated that NSC proliferation decreased with Aβ25-35 oligomer treatment; however, a combined treatment with candesartan restored it. Western blotting displayed that candesartan treatment increased the expression levels of p85α PI3K, pAkt (Ser473), pGSK-3β (Ser9), and HSTF. The NSCs were pretreated with a PI3K inhibitor, LY294002; the effects of candesartan on the proliferation of NSCs inhibited by Aβ25-35 oligomers were almost completely blocked. Conclusions Together, these results suggest that candesartan restores the Aβ25-35 oligomer-inhibited proliferation of NSCs by activating the PI3K pathway.en_US
dc.language.isoen_USen_US
dc.publisher대한치매학회en_US
dc.subjectcandesartanen_US
dc.subjectamyloid betaen_US
dc.subjectneural stem cellsen_US
dc.titleCandesartan Restores the Amyloid Beta-Inhibited Proliferation of Neural Stem Cells by Activating the Phosphatidylinositol 3-Kinase Pathwayen_US
dc.typeArticleen_US
dc.relation.no3-
dc.relation.volume16-
dc.relation.page64-71-
dc.relation.journalDementia and Neurocognitive Disorders(대한치매학회지)-
dc.contributor.googleauthor최호진-
dc.contributor.googleauthor최나영-
dc.contributor.googleauthor이규용-
dc.contributor.googleauthor이영주-
dc.contributor.googleauthor고성호-
dc.contributor.googleauthorChoi, Hojin-
dc.contributor.googleauthorChoi, Na-Young-
dc.contributor.googleauthorLee, Kyu-Yong-
dc.contributor.googleauthorLee, Young Joo-
dc.contributor.googleauthorKoh, Seong-Ho-
dc.relation.code2017019278-
dc.sector.campusS-
dc.sector.daehakCOLLEGE OF MEDICINE[S]-
dc.sector.departmentDEPARTMENT OF MEDICINE-
dc.identifier.pidyjlee1-


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