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|Title:||Formononetin, an isoflavone, relaxes rat isolated aorta through endothelium-dependent and endothelium-independent pathways|
Au, Alice Lai Shan
Poon, Christina Chui-Wa
Leung, George P. H.
Lee, Simon M. Y.
BK[sub ca] and K[sub ATP] channels
|Source:||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.|
|Rights:||Journal of Nutritional Biochemistry © 2010 Elsevier Inc. The journal web site is located at http://www.sciencedirect.com.|
|Appears in Collections:||ABCT Journal/Magazine Articles|
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