Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/40301
DC FieldValueLanguage
dc.contributor.authorSheu, M.L.en_US
dc.contributor.author許美鈴zh_TW
dc.contributor.authorChiang, C.K.en_US
dc.contributor.authorTsai, K.S.en_US
dc.contributor.authorHo, F.M.en_US
dc.contributor.authorWeng, T.I.en_US
dc.contributor.authorWu, H.Y.en_US
dc.contributor.authorLiu, S.H.en_US
dc.date2008zh_TW
dc.date.accessioned2014-06-06T08:03:34Z-
dc.date.available2014-06-06T08:03:34Z-
dc.identifier.issn0891-5849zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/40301-
dc.description.abstractAngiopathy is a major complication of diabetes. Abnormally high blood glucose is a crucial risk factor for endothelial cell damage. Nuclear factor-kappa B (NF-kappa B) has been demonstrated as a mediated signaling in hyperglycemia or oxidative stress-triggered apoptosis of endothelial cells. Here we explored the efficacy of honokiol, a small molecular weight natural product, on NADPH oxidase-related oxidative stress-mediated NF-kappa B-regulated signaling and apoptosis in human umbilical vein endothelial cells (HUVECs) under hyperglycemic conditions. The methods of morphological Hoechst staining and annexin V/propidium iodide staining were used to detect apoptosis. Submicromolar concentrations of honokiol suppressed the increases of NADPH oxidase activity, Rac-1 phosphorylation, p22(phox) protein expression, and reactive oxygen species production in high glucose (HG)-stimulated HUVECs. The degradation of I kappa B alpha and increase of NF-K beta activity were inhibited by honokiol in HG-treated HUVECs. Moreover, honokiol (0.125-1 mu M) also suppressed HG-induced cyclooxygenase (COX)-2 upregulation and prostaglandin E(2) production in HUVECs. Honokiol could reduce increased caspase-3 activity and the subsequent apoptosis and cell death triggered by HG. These results imply that inhibition of NADPH oxidase-related oxidative stress by honokiol suppresses the HG-induced NF-kappa B-regulated COX-2 upregulation, apoptosis, and cell death in HUVECs, which has the potential to be developed as a therapeutic agent to prevent hyperglycemia-induced endothelial damage. (C) 2008 Elsevier Inc. All rights reserved.en_US
dc.language.isoen_USzh_TW
dc.relationFree Radical Biology and Medicineen_US
dc.relation.ispartofseriesFree Radical Biology and Medicine, Volume 44, Issue 12, Page(s) 2043-2050.en_US
dc.subjecthonokiolen_US
dc.subjecthuman umbilical vein endothelial cellsen_US
dc.subjecthyperglycemiaen_US
dc.subjectNADPHen_US
dc.subjectoxidaseen_US
dc.subjectreactive oxygen speciesen_US
dc.subjectNF-kappa Ben_US
dc.subjectcyclooxygenase-2en_US
dc.subjectapoptosisen_US
dc.subjectnf-kappa-ben_US
dc.subjectischemia-reperfusion injuryen_US
dc.subjectoxygen species productionen_US
dc.subjectnitric-oxideen_US
dc.subjectcyclooxygenase-2 expressionen_US
dc.subjectp65 phosphorylationen_US
dc.subjectnatural-producten_US
dc.subjectmesangial cellsen_US
dc.subjectalpha kinaseen_US
dc.subjectdiabetic raten_US
dc.titleInhibition of NADPH oxidase-related oxidative stress-triggered signaling by honokiol suppresses high glucose-induced human endothelial cell apoptosisen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1016/j.freeradbiomed.2008.03.014zh_TW
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.fulltextno fulltext-
item.languageiso639-1en_US-
item.grantfulltextnone-
Appears in Collections:生物醫學研究所
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