Journal
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
Volume 394, Issue 2, Pages 217-226Publisher
SPRINGER
DOI: 10.1007/s00210-020-01953-8
Keywords
Mitochondria; Cardiac hypertrophy; Quercetin; Free radicals; Antioxidants
Categories
Funding
- UFCA
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
- Fundacao Cearense de Apoio ao Desenvolvimento Cientifico e Tecnologico (FUNCAP) [88887.166577/2018-01]
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico-CNPq [409489/2018-2]
- Centro de Pesquisa, Inovacao e Difusao de Processos Redox em Biomedicina [FAPESP 13/07937-8]
- CNPq
- CAPES
- UFCA (Edital ConsolidaPG)
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Quercetin is capable of attenuating cardiac hypertrophy by restoring cellular redox balance and protecting mitochondria.
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 H(2)O(2)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.
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