Quercetin prevents left ventricular hypertrophy in the Apo E knockout mouse

• 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
• ISSN: 2213-2317; 2213-2317
• DOI: 10.1016/j.redox.2013.07.001

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.