Quercetin prevents left ventricular hypertrophy in the Apo E knockout mouse

Hypercholesterolemia is a risk factor for the development of hypertrophic cardiomyopathy. Nevertheless, there are few studies aimed at determining the effects of dietary compounds on early or mild cardiac hypertrophy associated with dyslipidemia. Here we describe left ventricular (LV) hypertrophy in...

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Bibliographic Details
Published in:Redox biology 2013-01, Vol.1 (1), p.381-386
Main Authors: Ulasova, Elena, Perez, Jessica, Hill, Bradford G, Bradley, Wayne E, Garber, David W, Landar, Aimee, Barnes, Stephen, Prasain, Jeevan, Parks, Dale A, Dell'Italia, Louis J, Darley-Usmar, Victor M
Format: Article
Language:English
Subjects:
Animals
Antioxidants - administration & dosage
Antioxidants - therapeutic use
Apolipoproteins E - genetics
Atherosclerosis
Cholesterol
Cholesterol - blood
Hypercholesterolemia - diet therapy
Hypercholesterolemia - genetics
Hypercholesterolemia - pathology
Hypertrophy
Hypertrophy, Left Ventricular - complications
Hypertrophy, Left Ventricular - diet therapy
Hypertrophy, Left Ventricular - physiopathology
Mice
Mice, Inbred C57BL
Mice, Knockout
Quercetin
Quercetin - administration & dosage
Quercetin - therapeutic use
Ventricular Remodeling - drug effects
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Summary:Hypercholesterolemia is a risk factor for the development of hypertrophic cardiomyopathy. Nevertheless, there are few studies aimed at determining the effects of dietary compounds on early or mild cardiac hypertrophy associated with dyslipidemia. Here we describe left ventricular (LV) hypertrophy in 12 week-old Apo E(-/-) hypercholesterolemic mice. The LV end 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 µmol 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.
ISSN:2213-2317
2213-2317
DOI:10.1016/j.redox.2013.07.001