Quercetin treatment increases H 2 O 2 removal by restoration of endogenous antioxidant activity and blocks isoproterenol
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ORIGINAL ARTICLE
Quercetin treatment increases H2O2 removal by restoration of endogenous antioxidant activity and blocks isoproterenol-induced cardiac hypertrophy Joana Varlla de Lacerda Alexandre 1 & Yuana Ivia Ponte Viana 1 & Cícera Edna Barbosa David 1 & Pedro Lourenzo Oliveira Cunha 1 & Amanda Cabral Albuquerque 1 & Anna Lídia Nunes Varela 1 & Alicia J. Kowaltowski 2 & Heberty Tarso Facundo 1 Received: 24 May 2020 / Accepted: 20 July 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Oxidative stress, characterized by the accumulation of reactive oxygen species (ROS), is implicated in the pathogenesis of several diseases, including cardiac hypertrophy. The flavonoid quercetin is a potent ROS scavenger, with several beneficial effects for the cardiovascular system, including antihypertrophic effects. Oxidative imbalance has been implicated in cardiac hypertrophy and heart failure. In this work, we tested whether quercetin could attenuate cardiac hypertrophy by improving redox balance and mitochondrial homeostasis. To test this hypothesis, we treated a group of mice with isoproterenol (30 mg/kg/day) for 4 or 8 consecutive days. Another group received quercetin (10 mg/kg/day) from day 5th of isoproterenol treatment. We carried out the following assays in cardiac tissue: measurement of cardiac hypertrophy, protein sulfhydryl, catalase, Cu/Zn and Mn-superoxide dismutase (SOD) activity, detection of H2O2, and opening of the mitochondrial permeability transition pore. The animals treated with isoproterenol for the initial 4 days showed increased cardiac weight/tibia length ratio, decreased protein sulfhydryl content, compromised SOD and catalase activity, and high H2O2 levels. Quercetin was able to attenuate cardiac hypertrophy, restore protein sulfhydryl, and antioxidant activity, in addition to efficiently blocking the H2O2. We also observed that isoproterenol decreases mitochondrial SOD activity, while quercetin reverses it. Strikingly, quercetin also protects mitochondria against the opening of mitochondrial permeability transition pore. Taken together, these results suggest that quercetin is capable of reversing established isoproterenol-induced cardiac hypertrophy through the restoration of cellular redox balance and protecting mitochondria. Keywords Mitochondria . Cardiac hypertrophy . Quercetin . Free radicals . Antioxidants
Introduction Pathological hypertrophy occurs initially as an adaptive response in which differentiated cardiomyocytes grow, and changes in cardiac tissue occur to accommodate pressure or Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00210-020-01953-8) contains supplementary material, which is available to authorized users. * Heberty Tarso Facundo [email protected] 1
Faculdade de Medicina, Universidade Federal do Cariri, Barbalha, CE, Brazil
2
Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, SP, Brazil
volume overload. Although the heart is a dynamic organ, persis
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