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dc.contributor.authorKiyoshi Kikuchien_US
dc.contributor.authorKo Ichi Kawaharaen_US
dc.contributor.authorSalunya Tancharoenen_US
dc.contributor.authorFumiyo Matsudaen_US
dc.contributor.authorYoko Morimotoen_US
dc.contributor.authorTakashi Itoen_US
dc.contributor.authorKamal Krishna Biswasen_US
dc.contributor.authorKazunori Takenouchien_US
dc.contributor.authorNaoki Miuraen_US
dc.contributor.authorYoko Oyamaen_US
dc.contributor.authorYuko Nawaen_US
dc.contributor.authorNoboru Arimuraen_US
dc.contributor.authorMasahiro Iwataen_US
dc.contributor.authorYutaka Tajimaen_US
dc.contributor.authorTerukazu Kuramotoen_US
dc.contributor.authorKenji Nakayamaen_US
dc.contributor.authorMinoru Shigemorien_US
dc.contributor.authorYoshihiro Yoshidaen_US
dc.contributor.authorTeruto Hashiguchien_US
dc.contributor.authorIkuro Maruyamaen_US
dc.contributor.otherKagoshima University Faculty of Medicineen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherKagoshima Universityen_US
dc.contributor.otherOmuta City General Hospitalen_US
dc.contributor.otherKurume Universityen_US
dc.date.accessioned2018-09-13T06:24:18Z-
dc.date.available2018-09-13T06:24:18Z-
dc.date.issued2009-06-01en_US
dc.identifier.citationJournal of Pharmacology and Experimental Therapeutics. Vol.329, No.3 (2009), 865-874en_US
dc.identifier.issn15210103en_US
dc.identifier.issn00223565en_US
dc.identifier.other2-s2.0-66749132080en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=66749132080&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/27216-
dc.description.abstractEdaravone, a potent free radical scavenger, is clinically used for the treatment of cerebral infarction in Japan. Here, we examined the effects of edaravone on the dynamics of high-mobility group box-1 (HMGB1), which is a key mediator of ischemic-induced brain damage, during a 48-h postischemia/ reperfusion period in rats and in oxygen-glucose-deprived (OGD) PC12 cells. HMGB1 immunoreactivity was observed in both the cytoplasm and the periphery of cells in the cerebral infarction area 2 h after reperfusion. Intravenous administration of 3 and 6 mg/kg edaravone significantly inhibited nuclear translocation and HMGB1 release in the penumbra area and caused a 26.5 ± 10.4 and 43.8 ± 0.5% reduction, respectively, of the total infarct area at 24 h after reperfusion. Moreover, edaravone also decreased plasma HMGB1 levels. In vitro, edaravone dose-dependently (1-10 μM) suppressed OGD- and H2O2-induced HMGB1 release in PC12 cells. Furthermore, edaravone (3-30 μM) blocked HMGB1-triggered apoptosis in PC12 cells. Our findings suggest a novel neuroprotective mechanism for edaravone that abrogates the release of HMGB1. Copyright © 2009 by The American Society for Pharmacology and Experimental Therapeutics.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=66749132080&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.subjectPharmacology, Toxicology and Pharmaceuticsen_US
dc.titleThe free radical scavenger edaravone rescues rats from cerebral infarction by attenuating the release of high-mobility group box-1 in neuronal cellsen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1124/jpet.108.149484en_US
Appears in Collections:Scopus 2006-2010

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