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Cardiovascular Research 2002 53(4):1010-1018; doi:10.1016/S0008-6363(01)00535-1
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Chronic antioxidant supplementation attenuates nuclear factor-{kappa}B activation and preserves endothelial function in hypercholesterolemic pigs

Martin Rodriguez-Porcela, Lilach O Lermanb, David R Holmes, Jr.a, Darcy Richardsona, Claudio Napolic,d and Amir Lermana,*

aDepartment of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
bDepartment of Internal Medicine, Division of Hypertension, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
cDepartment of Medicine, University of Naples, Naples, Italy
dDepartment of Medicine—0682, University of California, San Diego, CA, USA

* Corresponding author. Tel.: +1-507-255-4152; fax: +1-507-255-2550 lerman.amir{at}mayo.edu

Objective: Hypercholesterolemia (HC), a pro-oxidant condition, activates nuclear factor-kappa beta (NF-{kappa}B) and is associated with coronary endothelial dysfunction. The physiological significance of in vivo chronic antioxidant intervention on HC-induced NF-{kappa}B activation and coronary endothelial function remains unclear. Methods: Four groups of pigs were studied after 12 weeks of normal diet, normal diet with concomitant antioxidant intervention (100 IU/kg of vitamin E and 1 g of vitamin C daily), 2% HC diet, or HC diet+antioxidant supplementation. NF-{kappa}B activation and the nitric oxide (NO) pathway were investigated by Western blotting and immunohistochemistry, while oxidative stress was evaluated by coronary artery tissue radical scavenger activity and levels of vitamin E and C. Endothelial function was studied in vitro by coronary vasoreactivity to bradykinin and substance P. Results: HC animals had increased activation of NF-{kappa}B, decreased endothelial NO synthase expression, and decreased radical scavenger system activity, associated with impaired coronary endothelial function. Antioxidant supplementation in HC normalized NF-{kappa}B activation and NO bioactivity, and preserves coronary endothelial function. Conclusions: This study demonstrates for the first time that in vivo chronic interruption of the endogenous oxidative stress cascade reduces HC-induced NF-{kappa}B activation and normalizes NO bioactivity in association with preservation of coronary endothelial function. This study suggests a role for increased oxidative stress and NF{kappa}B activation in early atherosclerosis.

KEYWORDS Atherosclerosis; Coronary circulation; Endothelial function; Free radicals


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