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Article: Formononetin, an isoflavone, relaxes rat isolated aorta through endothelium-dependent and endothelium-independent pathways
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TitleFormononetin, an isoflavone, relaxes rat isolated aorta through endothelium-dependent and endothelium-independent pathways
 
AuthorsWu, JH3
Li, Q3 4
Wu, MY3
Guo, DJ3
Chen, HL3
Chen, SL3 4
Seto, SW6
Au, ALS6
Poon, CCW6
Leung, GPH1
Lee, SMY2
Kwan, YW6
Chan, SW3 5
 
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
 
CitationJournal Of Nutritional Biochemistry, 2010, v. 21 n. 7, p. 613-620 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.jnutbio.2009.03.010
 
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.
 
ISSN0955-2863
2012 Impact Factor: 4.552
2012 SCImago Journal Rankings: 1.262
 
DOIhttp://dx.doi.org/10.1016/j.jnutbio.2009.03.010
 
ISI Accession Number IDWOS:000279363200007
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.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorWu, JH
 
dc.contributor.authorLi, Q
 
dc.contributor.authorWu, MY
 
dc.contributor.authorGuo, DJ
 
dc.contributor.authorChen, HL
 
dc.contributor.authorChen, SL
 
dc.contributor.authorSeto, SW
 
dc.contributor.authorAu, ALS
 
dc.contributor.authorPoon, CCW
 
dc.contributor.authorLeung, GPH
 
dc.contributor.authorLee, SMY
 
dc.contributor.authorKwan, YW
 
dc.contributor.authorChan, SW
 
dc.date.accessioned2010-10-19T07:44:56Z
 
dc.date.available2010-10-19T07:44:56Z
 
dc.date.issued2010
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationJournal Of Nutritional Biochemistry, 2010, v. 21 n. 7, p. 613-620 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.jnutbio.2009.03.010
 
dc.identifier.citeulike5368459
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.jnutbio.2009.03.010
 
dc.identifier.epage620
 
dc.identifier.hkuros172612
 
dc.identifier.isiWOS:000279363200007
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.

 
dc.identifier.issn0955-2863
2012 Impact Factor: 4.552
2012 SCImago Journal Rankings: 1.262
 
dc.identifier.issue7
 
dc.identifier.openurl
 
dc.identifier.pmid19570671
 
dc.identifier.scopuseid_2-s2.0-77953812949
 
dc.identifier.spage613
 
dc.identifier.urihttp://hdl.handle.net/10722/124066
 
dc.identifier.volume21
 
dc.languageeng
 
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jnutbio
 
dc.publisher.placeUnited States
 
dc.relation.ispartofJournal of Nutritional Biochemistry
 
dc.relation.referencesReferences in Scopus
 
dc.rightsThe Journal of Nutritional Biochemistry. Copyright © Elsevier Inc.
 
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.subjectBK Ca and K ATP channels
 
dc.subjectFormononetin
 
dc.subjectNitric oxide
 
dc.subjectVasorelaxation
 
dc.titleFormononetin, an isoflavone, relaxes rat isolated aorta through endothelium-dependent and endothelium-independent pathways
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong
  2. University of Macau
  3. State Key Laboratory of Chinese Medicine and Molecular Pharmacology
  4. Chinese Academy of Medical Sciences
  5. Hong Kong Polytechnic University
  6. Chinese University of Hong Kong