PolyU IR

PolyU Institutional Repository >
Applied Biology and Chemical Technology >
ABCT Journal/Magazine Articles >

Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/2374

Title: Formononetin, an isoflavone, relaxes rat isolated aorta through endothelium-dependent and endothelium-independent pathways
Authors: Wu, Jianhong
Li, Qing
Wu, Minyi
Guo, Dejian
Chen, Huan-Le
Chen, Shilin
Seto, Sai-Wang
Au, Alice Lai Shan
Poon, Christina Chui-Wa
Leung, George P. H.
Lee, Simon M. Y.
Kwan, Yiu-Wa
Chan, Shun-wan
Subjects: Formononetin
Nitric oxide
BK[sub ca] and K[sub ATP] channels
Issue Date: Jul-2010
Publisher: Elsevier
Citation: Journal of nutritional biochemistry, July 2010, v. 21, no. 7, p. 613-620.
Abstract: We 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[sup Ser]¹¹ ⁷ ⁷ 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 Ca²⁺-activated K⁺ (BK[sub ca]) channels and glibenclamide-sensitive adenosine triphosphate (ATP)- dependent K⁺ (K[sub 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[sub ca] and K[sub ATP] channels.
Description: DOI: 10.1016/j.jnutbio.2009.03.010
Rights: Journal of Nutritional Biochemistry © 2010 Elsevier Inc. The journal web site is located at http://www.sciencedirect.com.
Type: Journal/Magazine Article
URI: http://hdl.handle.net/10397/2374
ISSN: 0955-2863
Appears in Collections:ABCT Journal/Magazine Articles

Files in This Item:

File Description SizeFormat
Formononetin (Final).pdfPre-published version900.67 kBAdobe PDFView/Open
Locate publisher version via PolyU eLinks

Facebook Facebook del.icio.us del.icio.us LinkedIn LinkedIn

All items in the PolyU Institutional Repository are protected by copyright, with all rights reserved, unless otherwise indicated.
No item in the PolyU IR may be reproduced for commercial or resale purposes.


© Pao Yue-kong Library, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong
Powered by DSpace (Version 1.5.2)  © MIT and HP
Feedback | Privacy Policy Statement | Copyright & Restrictions - Feedback