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Oxidative Medicine and Cellular Longevity
Volume 2018, Article ID 7239123, 14 pages
Research Article

Quercetin Prevents Diastolic Dysfunction Induced by a High-Cholesterol Diet: Role of Oxidative Stress and Bioenergetics in Hyperglycemic Rats

1Pathophysiology Program, ICBM, Faculty of Medicine, University of Chile, Av. Salvador 486, Providencia, 7500922 Santiago, Chile
2International Center for Andean Studies, Universidad de Chile, Putre, Chile
3Department of Nutrition, Faculty of Medicine, University of Chile, Santiago, Chile
4Universidad de Viña del Mar, Región de Valparaíso, Chile
5Centro de Simulación Clínica, Universidad Iberoamericana, Santiago, Chile
6Servicios Médicos Veterinarios de Especialidad-VETCO, Santiago, Chile
7Discovery Biology, Griffith Institute for Drug Discovery, Griffith University, Nathan, QLD 4111, Australia

Correspondence should be addressed to Catalina Carrasco-Pozo; moc.liamg@opacatac

Received 6 August 2017; Accepted 23 October 2017; Published 11 January 2018

Academic Editor: Vladimir Jakovljevic

Copyright © 2018 Rodrigo L. Castillo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Alterations in cardiac energy metabolism play a key role in the pathogenesis of diabetic cardiomyopathy. Hypercholesterolemia associated with bioenergetic impairment and oxidative stress has not been well characterized in the cardiac function under glycemic control deficiency conditions. This work aimed to determine the cardioprotective effects of quercetin (QUE) against the damage induced by a high-cholesterol (HC) diet in hyperglycemic rats, addressing intracellular antioxidant mechanisms and bioenergetics. Quercetin reduced HC-induced alterations in the lipid profile and glycemia in rats. In addition, QUE attenuated cardiac diastolic dysfunction (increased E:A ratio), prevented cardiac cholesterol accumulation, and reduced the increase in HC-induced myocyte density. Moreover, QUE reduced HC-induced oxidative stress by preventing the decrease in GSH/GSSG ratio, Nrf2 nuclear translocation, HO-1 expression, and antioxidant enzymatic activity. Quercetin also counteracted HC-induced bioenergetic impairment, preventing a reduction in ATP levels and alterations in PGC-1α, UCP2, and PPARγ expression. In conclusion, the mechanisms that support the cardioprotective effect of QUE in rats with HC might be mediated by the upregulation of antioxidant mechanisms and improved bioenergetics on the heart. Targeting bioenergetics with QUE can be used as a pharmacological approach to modulate structural and functional changes of the heart under hypercholesterolemic and hyperglycemic conditions.