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Article: Formononetin, an isoflavone, relaxes rat isolated aorta through endothelium-dependent and endothelium-independent pathways

TitleFormononetin, an isoflavone, relaxes rat isolated aorta through endothelium-dependent and endothelium-independent pathways
Authors
KeywordsBK Ca and K ATP channels
Formononetin
Nitric oxide
Vasorelaxation
Issue Date2010
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jnutbio
Citation
Journal Of Nutritional Biochemistry, 2010, v. 21 n. 7, p. 613-620 How to Cite?
AbstractWe evaluated the vasorelaxation effects of formononetin, an isoflavone/phytoestrogen found abundantly in Astragalus mongholicus Bunge, on rat isolated aorta and the underlying mechanisms involved. Cumulative administration of formononetin, genistein, daidzein and biochanin A relaxed phenylephrine-preconstricted aorta. Formononetin and biochanin A caused a similar magnitude of relaxation whereas daidzein was least potent. Mechanical removal of endothelium, L-NAME (100 μM) and methylene blue (10 μM) suppressed formononetin-induced relaxation. Formononetin increased endothelial nitric oxide (NO) synthase (eNOS), but not inducible NO synthase, activity with an up-regulation of eNOS mRNA and p-eNOS Ser1177 protein expression. In endothelium-denuded preparations, formononetin-induced vasorelaxation was significantly reduced by glibenclamide (3 μM) and iberiotoxin (100 nM), and a combination of glibenclamide (3 μM) plus iberiotoxin (100 nM) abolished the relaxation. In contrast, formononetin-elicited endothelium-independent relaxation was not altered by ICI 182,780 (10 μM, an estrogen receptor (ERα/ERβ) antagonist) or mifepristone (10 μM, a progesterone receptor antagonist). In single aortic smooth muscle cells, formononetin caused opening of iberiotoxin-sensitive Ca 2+-activated K + (BK Ca) channels and glibenclamide-sensitive adenosine triphosphate (ATP)-dependent K + (K ATP) channels. Thus, our results suggest that formononetin caused vascular relaxation via endothelium/NO-dependent mechanism and endothelium-independent mechanism which involves the activation of BK Ca and K ATP channels. © 2010 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/124066
ISSN
2015 Impact Factor: 4.668
2015 SCImago Journal Rankings: 1.886
ISI Accession Number ID
Funding AgencyGrant Number
"Shenzhen Virtual University Park," Shenzhen Government (PR China)
Hong Kong Polytechnic University
Direct Grants for Research (The Chinese University of Hong Kong)2401149
2041231
2401296
Hong Kong SAR4107/01M
4166/02M
2140565
Department of Pharmacology (The Chinese University of Hong Kong, Hong Kong SAR)
Funding Information:

We are grateful to assistance provided by technicians of State Key Laboratory of Chinese Medicine and Molecular Pharmacology, Department of Applied Biology and Chemical Technology, Hong Kong Polytechnic University (Hong Kong SAR, PR China). This project was supported by a research grant of the "Shenzhen Virtual University Park," Shenzhen Government (PR China), the Niche Area Research Grant of the Hong Kong Polytechnic University, Direct Grants for Research (The Chinese University of Hong Kong) (Reference No.: 2401149; Project code: 2041231; 2401296), and the RGC Earmarked Grants of Hong Kong SAR (Ref. #: 4107/01M; 4166/02M, project code: 2140565). Mr. Sai-Wang Seto and Ms. Alice L.S. Au are recipients of the post-graduate studentship of the Department of Pharmacology (The Chinese University of Hong Kong, Hong Kong SAR). Proofreading of the manuscript by Mr. Ho-Yeung Lam is also acknowledged.

References

 

DC FieldValueLanguage
dc.contributor.authorWu, JHen_HK
dc.contributor.authorLi, Qen_HK
dc.contributor.authorWu, MYen_HK
dc.contributor.authorGuo, DJen_HK
dc.contributor.authorChen, HLen_HK
dc.contributor.authorChen, SLen_HK
dc.contributor.authorSeto, SWen_HK
dc.contributor.authorAu, ALSen_HK
dc.contributor.authorPoon, CCWen_HK
dc.contributor.authorLeung, GPHen_HK
dc.contributor.authorLee, SMYen_HK
dc.contributor.authorKwan, YWen_HK
dc.contributor.authorChan, SWen_HK
dc.date.accessioned2010-10-19T07:44:56Z-
dc.date.available2010-10-19T07:44:56Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Nutritional Biochemistry, 2010, v. 21 n. 7, p. 613-620en_HK
dc.identifier.issn0955-2863en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124066-
dc.description.abstractWe evaluated the vasorelaxation effects of formononetin, an isoflavone/phytoestrogen found abundantly in Astragalus mongholicus Bunge, on rat isolated aorta and the underlying mechanisms involved. Cumulative administration of formononetin, genistein, daidzein and biochanin A relaxed phenylephrine-preconstricted aorta. Formononetin and biochanin A caused a similar magnitude of relaxation whereas daidzein was least potent. Mechanical removal of endothelium, L-NAME (100 μM) and methylene blue (10 μM) suppressed formononetin-induced relaxation. Formononetin increased endothelial nitric oxide (NO) synthase (eNOS), but not inducible NO synthase, activity with an up-regulation of eNOS mRNA and p-eNOS Ser1177 protein expression. In endothelium-denuded preparations, formononetin-induced vasorelaxation was significantly reduced by glibenclamide (3 μM) and iberiotoxin (100 nM), and a combination of glibenclamide (3 μM) plus iberiotoxin (100 nM) abolished the relaxation. In contrast, formononetin-elicited endothelium-independent relaxation was not altered by ICI 182,780 (10 μM, an estrogen receptor (ERα/ERβ) antagonist) or mifepristone (10 μM, a progesterone receptor antagonist). In single aortic smooth muscle cells, formononetin caused opening of iberiotoxin-sensitive Ca 2+-activated K + (BK Ca) channels and glibenclamide-sensitive adenosine triphosphate (ATP)-dependent K + (K ATP) channels. Thus, our results suggest that formononetin caused vascular relaxation via endothelium/NO-dependent mechanism and endothelium-independent mechanism which involves the activation of BK Ca and K ATP channels. © 2010 Elsevier Inc.en_HK
dc.languageeng-
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jnutbioen_HK
dc.relation.ispartofJournal of Nutritional Biochemistryen_HK
dc.rightsThe Journal of Nutritional Biochemistry. Copyright © Elsevier Inc.-
dc.subjectBK Ca and K ATP channelsen_HK
dc.subjectFormononetinen_HK
dc.subjectNitric oxideen_HK
dc.subjectVasorelaxationen_HK
dc.subject.meshAorta, Thoracic-
dc.subject.meshEndothelium, Vascular - drug effects - physiology-
dc.subject.meshIsoflavones - pharmacology-
dc.subject.meshVasodilation - drug effects-
dc.subject.meshVasodilator Agents - pharmacology-
dc.titleFormononetin, an isoflavone, relaxes rat isolated aorta through endothelium-dependent and endothelium-independent pathwaysen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0955-2863&volume=21&issue=7&spage=613&epage=620&date=2010&atitle=Formononetin,+an+isoflavone,+relaxes+rat+isolated+aorta+through+endothelium-dependent+and+endothelium-independent+pathways-
dc.identifier.emailLeung, GPH: gphleung@hkucc.hku.hken_HK
dc.identifier.authorityLeung, GPH=rp00234en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jnutbio.2009.03.010en_HK
dc.identifier.pmid19570671-
dc.identifier.scopuseid_2-s2.0-77953812949en_HK
dc.identifier.hkuros172612-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77953812949&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume21en_HK
dc.identifier.issue7en_HK
dc.identifier.spage613en_HK
dc.identifier.epage620en_HK
dc.identifier.isiWOS:000279363200007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWu, JH=35313190600en_HK
dc.identifier.scopusauthoridLi, Q=26643058000en_HK
dc.identifier.scopusauthoridWu, MY=7405595237en_HK
dc.identifier.scopusauthoridGuo, DJ=20436287700en_HK
dc.identifier.scopusauthoridChen, HL=36559136500en_HK
dc.identifier.scopusauthoridChen, SL=7410258549en_HK
dc.identifier.scopusauthoridSeto, SW=9941482400en_HK
dc.identifier.scopusauthoridAu, ALS=7005391144en_HK
dc.identifier.scopusauthoridPoon, CCW=26656895800en_HK
dc.identifier.scopusauthoridLeung, GPH=35963668200en_HK
dc.identifier.scopusauthoridLee, SMY=35233892600en_HK
dc.identifier.scopusauthoridKwan, YW=7005662153en_HK
dc.identifier.scopusauthoridChan, SW=7404255670en_HK
dc.identifier.citeulike5368459-

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