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Article: Berberine prevents hyperglycemia-induced endothelial injury and enhances vasodilatation via adenosine monophosphate-activated protein kinase and endothelial nitric oxide synthase

TitleBerberine prevents hyperglycemia-induced endothelial injury and enhances vasodilatation via adenosine monophosphate-activated protein kinase and endothelial nitric oxide synthase
Authors
KeywordsEndothelium
Hyperglycemia
Nitric oxide
Oxidative stress
Vascular injury
Issue Date2009
PublisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
Citation
Cardiovascular Research, 2009, v. 82 n. 3, p. 484-492 How to Cite?
AbstractAimsEndothelial dysfunction is a key event that links obesity, diabetes, hypertension, and cardiovascular diseases. The aim of the present study was to examine the protective effect of the alkaloid drug berberine against hyperglycemia-induced cellular injury and endothelial dysfunction.Methods and resultsIn both cultured endothelial cells and blood vessels isolated from rat aorta, berberine concentration dependently enhanced phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser 1177 and promoted the association of eNOS with heat shock protein 90 (HSP90), leading to an increased production of nitric oxide. Furthermore, berberine attenuated high glucose-induced generation of reactive oxygen species, cellular apoptosis, nuclear factor-κB activation, and expression of adhesion molecules, thus suppressing monocyte attachment to endothelial cells. In mouse aortic rings, berberine elicited endothelium-dependent vasodilatations and alleviated high glucose-mediated endothelial dysfunction. All these beneficial effects of berberine on the endothelium were abolished by either pharmacological inhibition of adenosine monophosphate-activated protein kinase (AMPK) or adenovirus-mediated overexpression of a dominant negative version of AMPK.ConclusionBerberine protects against endothelial injury and enhances the endothelium-dependent vasodilatation, which is mediated in part through activation of the AMPK signalling cascade. Berberine or its derivatives may be useful for the treatment and/or prevention of endothelial dysfunction associated with diabetes and cardiovascular disease.
Persistent Identifierhttp://hdl.handle.net/10722/76604
ISSN
2015 Impact Factor: 5.465
2015 SCImago Journal Rankings: 2.897
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grant CouncilHKU 7645/06M
CUHK 4653/08
Collaborative Research FundHKU 2/07C
University of Hong Kong
Funding Information:

This work was supported by Hong Kong Research Grant Council (HKU 7645/06M to A. X. and CUHK 4653/08 to Y. H.) and Collaborative Research Fund (HKU 2/07C), the outstanding Young researcher award from University of Hong Kong (to A. X.).

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_HK
dc.contributor.authorHuang, Yen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorLi, Yen_HK
dc.contributor.authorWong, WTen_HK
dc.contributor.authorYe, Hen_HK
dc.contributor.authorLau, CWen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorXu, Aen_HK
dc.date.accessioned2010-09-06T07:23:00Z-
dc.date.available2010-09-06T07:23:00Z-
dc.date.issued2009en_HK
dc.identifier.citationCardiovascular Research, 2009, v. 82 n. 3, p. 484-492en_HK
dc.identifier.issn0008-6363en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76604-
dc.description.abstractAimsEndothelial dysfunction is a key event that links obesity, diabetes, hypertension, and cardiovascular diseases. The aim of the present study was to examine the protective effect of the alkaloid drug berberine against hyperglycemia-induced cellular injury and endothelial dysfunction.Methods and resultsIn both cultured endothelial cells and blood vessels isolated from rat aorta, berberine concentration dependently enhanced phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser 1177 and promoted the association of eNOS with heat shock protein 90 (HSP90), leading to an increased production of nitric oxide. Furthermore, berberine attenuated high glucose-induced generation of reactive oxygen species, cellular apoptosis, nuclear factor-κB activation, and expression of adhesion molecules, thus suppressing monocyte attachment to endothelial cells. In mouse aortic rings, berberine elicited endothelium-dependent vasodilatations and alleviated high glucose-mediated endothelial dysfunction. All these beneficial effects of berberine on the endothelium were abolished by either pharmacological inhibition of adenosine monophosphate-activated protein kinase (AMPK) or adenovirus-mediated overexpression of a dominant negative version of AMPK.ConclusionBerberine protects against endothelial injury and enhances the endothelium-dependent vasodilatation, which is mediated in part through activation of the AMPK signalling cascade. Berberine or its derivatives may be useful for the treatment and/or prevention of endothelial dysfunction associated with diabetes and cardiovascular disease.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.orgen_HK
dc.relation.ispartofCardiovascular Researchen_HK
dc.subjectEndotheliumen_HK
dc.subjectHyperglycemiaen_HK
dc.subjectNitric oxideen_HK
dc.subjectOxidative stressen_HK
dc.subjectVascular injuryen_HK
dc.subject.meshAMP-Activated Protein Kinases - metabolism-
dc.subject.meshBerberine - pharmacology - therapeutic use-
dc.subject.meshEndothelial Cells - drug effects - enzymology-
dc.subject.meshHyperglycemia - drug therapy - metabolism-
dc.subject.meshNitric Oxide Synthase Type III - metabolism-
dc.titleBerberine prevents hyperglycemia-induced endothelial injury and enhances vasodilatation via adenosine monophosphate-activated protein kinase and endothelial nitric oxide synthaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-6363&volume=82&issue=3&spage=484&epage=492&date=2009&atitle=Berberine+prevents+hyperglycemia-induced+endothelial+injury+and+enhances+vasodilatation+via+adenosine+monophosphate-activated+protein+kinase+and+endothelial+nitric+oxide+synthaseen_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/cvr/cvp078en_HK
dc.identifier.pmid19251722-
dc.identifier.scopuseid_2-s2.0-66249092436en_HK
dc.identifier.hkuros169354en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-66249092436&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume82en_HK
dc.identifier.issue3en_HK
dc.identifier.spage484en_HK
dc.identifier.epage492en_HK
dc.identifier.isiWOS:000266109900015-
dc.publisher.placeUnited Kingdomen_HK
dc.relation.projectnull-
dc.relation.projectVascular dysfunction in obesity and diabetes: from risk prediction to therapeutic intervention-
dc.identifier.scopusauthoridWang, Y=13104237500en_HK
dc.identifier.scopusauthoridHuang, Y=34770945300en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridLi, Y=8605315400en_HK
dc.identifier.scopusauthoridWong, WT=35932584500en_HK
dc.identifier.scopusauthoridYe, H=7201887749en_HK
dc.identifier.scopusauthoridLau, CW=7401968520en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.citeulike8383496-

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