Quercetin treatment increases H(2)O(2)removal by restoration of endogenous antioxidant activity and blocks isoproterenol-induced cardiac hypertrophy

Autor(es)

de Lacerda Alexandre, Joana Varlla ^[1] ; Viana, Yuana Ivia Ponte ^[1] ; David, Cicera Edna Barbosa ^[1] ; Cunha, Pedro Lourenzo Oliveira ^[1] ; Albuquerque, Amanda Cabral ^[1] ; Varela, Anna Lidia Nunes ^[1] ; Kowaltowski, Alicia J. ^[2] ; Facundo, Heberty Tarso ^[1]

Afiliação do(s) autor(es)

^[1] Univ Fed Cariri, Fac Med, Barbalha, CE - Brazil

^[2] Univ Sao Paulo, Inst Quim, Dept Bioquim, Sao Paulo, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY; v. 394, n. 2, p. 217-226, FEB 2021.
• Citações Web of Science: 2

Resumo

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. (AU)

• Processo FAPESP: 13/07937-8 - Redoxoma
• Beneficiário: Ohara Augusto
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs