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dc.contributor.author오세관-
dc.contributor.author정재철-
dc.date.accessioned2017-08-28T20:04:23Z-
dc.date.available2017-08-28T20:04:23Z-
dc.date.issued2009-
dc.identifier.issn0022-3565-
dc.identifier.otherOAK-5346-
dc.identifier.urihttp://dspace.ewha.ac.kr/handle/2015.oak/231879-
dc.description.abstractTo search for new neuroprotective compounds, novel benzylideneacetophenone compounds (JCI, (3E)-4-(4-hydroxy-3-methoxyphenyl)but-3-en-2-one; JC2, (1E)-1-(4-hydroxy-3-methoxyphenyl)hept-1-en-3-one; JC3, (2E)-3-(4-hydroxy-3- methoxyphenyl)phenylpro-2-en-l-one; JC4, (1E)-1-(4-hydroxy-3-methoxyphenyl)-5- phenylpent-1-en-3-one; JC5, (1E)-3-(4-hydroxy-3-methoxyphenyl)-6-phenylhex-1-en- 3-one; JC6, (1E)-1-(4-hydroxy-3-methoxyphenyl]-7-phenylhept-1-en-3-one) were synthesized, and their potential to prevent neurotoxicities were evaluated. All compounds (JC1-JC6) showed considerable effect on free radical scavenging, the inhibition of glutamate-induced neurotoxicity in cortical cells, and the suppression of lipopolysaccharide (LPS)-induced nitric oxide (NO) generation in microglia. (2E)-3-(4-Hydroxy-3-methoxyphenyl)-phenylpro-2-en-1-one (JC3) exhibited the most potent neuroprotective effect in ischemia model using organotypic hippocampal culture and middle cerebral artery occlusion (MCAO). Based on the above-mentioned results, the mechanisms underlying the biological activity of JC3, which exhibited potent antiexcitotoxic and anti-inflammatory effects, were determined using cortical neuronal cells and microglia. Compound JC3 exerted a neuroprotective effect on oxygen-glucose deprivation- and hydrogen peroxide-induced cytotoxicity in cultured cortical cells. In addition, it suppressed the generation of NO, proinflammatory cytokines, and reactive oxygen species in LPS-treated microglial cells. It also suppressed the activation of phosphorylated Janus tyrosine kinase 2/phosphorylated signal transducer and activator of transcription 3 and mitogen-activated protein kinase (MAPK) in activated microglia and in cortex and striatum after 3 days of the MCAO in mice. These results demonstrated that JC3 might affect a set of intracellular signaling cascades, including the Janus tyrosine kinase/signal transducers and activators of transcription and MAPK pathways. This study suggests that benzylideneacetophenone derivative could be useful antineurotoxic agents. Copyright © 2009 by The American Society for Pharmacology and Experimental Therapeutics.-
dc.languageEnglish-
dc.titleThe neuroprotective effects of benzylideneacetophenone derivatives on excitotoxicity and inflammation via phosphorylated Janus tyrosine kinase 2/phosphorylated signal transducer and activator of transcription 3 and mitogen-activated protein K pathways-
dc.typeArticle-
dc.relation.issue2-
dc.relation.volume328-
dc.relation.indexSCI-
dc.relation.indexSCIE-
dc.relation.indexSCOPUS-
dc.relation.startpage435-
dc.relation.lastpage447-
dc.relation.journaltitleJournal of Pharmacology and Experimental Therapeutics-
dc.identifier.doi10.1124/jpet.108.144014-
dc.identifier.wosidWOS:000262623600009-
dc.identifier.scopusid2-s2.0-59649107514-
dc.author.googleJang S.-
dc.author.googleJung J.-C.-
dc.author.googleDong H.K.-
dc.author.googleJong H.R.-
dc.author.googleLee Y.-
dc.author.googleJung M.-
dc.author.googleOh S.-
dc.contributor.scopusid오세관(7404103757)-
dc.date.modifydate20180403152758-
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의과대학 > 의학과 > Journal papers
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