Journal
REDOX BIOLOGY
Volume 1, Issue 1, Pages 381-386Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.redox.2013.07.001
Keywords
Atherosclerosis; Hypertrophy; Cholesterol; Quercetin
Categories
Funding
- National Institutes of Health [HL070610]
- SCCOR in Cardiac Dysfunction [HL077100]
- Shared Instrumentation grant from the National Center for Research Resources [S10 RR19231]
- UAB Comprehensive Cancer Center [P30, CA13148-35]
- NATIONAL CANCER INSTITUTE [P30CA013148] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [S10RR019231] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL070610, P50HL077100] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK079626] Funding Source: NIH RePORTER
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Hypercholesterolemia is a risk factor for the development of hypertrophic carcliomyopathy. Nevertheless, there are few studies aimed at determining the effects of dietary compounds on early or mild cardiac hypertrophy associated with clyslipidemia. Here we describe left ventricular (LV) hypertrophy in 12 week-old Apo E-/- hypercholesterolemic mice. The LVend diastolic posterior wall thickness and overall LV mass were significantly increased in Apo E-/- mice compared with wild type (WT) controls. Fractional shortening, LV end diastolic diameter, and hemodynamic parameters were unchanged from WT mice. Oral low dose quercetin (QCN; 0.1 mu mol QCN/kg body weight for 6 weeks) significantly reduced total cholesterol and very low density lipoprotein in the plasma of Apo E-/- mice. QCN treatment also significantly decreased LV posterior wall thickness and LV mass in Apo E-/- mice. Myocardial geometry and function were unaffected in WT mice by QCN treatment. These data suggest that dietary polyphenolic compounds such as QCN may be effective modulators of plasma cholesterol and could prevent maladaptive myocardial remodeling. (C) 2013 The Authors. Published by Elsevier B.V. Open access under CC BY-N-C-SA license.
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