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Am J Physiol Heart Circ Physiol 289: H908-H915, 2005. First published April 1, 2005; doi:10.1152/ajpheart.00781.2004
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Revealing anti-inflammatory mechanisms of soy isoflavones by flow: modulation of leukocyte-endothelial cell interactions

Balu K. Chacko,1 Robert T. Chandler,1 Ameya Mundhekar,1 Nicholas Khoo,3 Heather M. Pruitt,1 Dennis F. Kucik,1,6 Dale A. Parks,3,5 Christopher G. Kevil,7 Stephen Barnes,2,4 and Rakesh P. Patel1,4,5

Departments of 1Pathology, 2Pharmacology, and 3Anesthesiology, 4Purdue-University of Alabama at Birmingham Botanical Center for Age-Related Disease, and 5Center for Free Radical Biology, University of Alabama at Birmingham; and 6Research Service, Birmingham Veterans Affairs Medical Center, Birmingham, Alabama; and 7Department of Pathology, Louisiana State University, Shreveport, Louisiana

Submitted 2 August 2004 ; accepted in final form 28 March 2005

The antiatherogenic effects of soy isoflavone consumption have been demonstrated in a variety of studies. However, the mechanisms involved remain poorly defined. Adhesion of monocytes to vascular endothelial cells is a key step within the inflammatory cascade that leads to atherogenesis. Many factors, including the physical forces associated with blood flow, regulate this process. Using an in vitro flow assay, we report that genistein, a principal component of most isoflavone preparations, inhibits monocyte adhesion to cytokine (TNF-{alpha})-stimulated human vascular endothelial cells at physiologically relevant concentrations (0–1 µM). This effect is absolutely dependent on flow and is not observed under static conditions. Furthermore, this inhibition was dependent on activation of endothelial peroxisomal proliferator-activated receptor-{gamma}. No significant role for other reported properties of genistein, including antioxidant effects, inhibition of tyrosine kinases, or activation of estrogen receptors, was observed. Furthermore, the antiadhesive effects of genistein did not occur via modulation of the adhesion molecules E-selectin, ICAM-1, VCAM-1, or platelet-endothelial cell adhesion molecule-1. These data reveal a novel anti-inflammatory mechanism for isoflavones and identify the physical forces associated with blood flow and a critical mediator of this function.

inflammation; genistein; peroxisomal proliferator-activated receptor-{gamma}; atherosclerosis; monocytes


Address for reprint requests and other correspondence: R. P. Patel, Dept. of Pathology, Univ. of Alabama at Birmingham, 901 19th St. South, BMR-2, Rm. 307, Birmingham, AL 35294 (E-mail: patel{at}path.uab.edu)




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