Banca de DEFESA: JOANA VARLLA DE LACERDA ALEXANDRE

Uma banca de DEFESA de MESTRADO foi cadastrada pelo programa.
DISCENTE : JOANA VARLLA DE LACERDA ALEXANDRE
DATA : 27/01/2020
HORA: 14:00
LOCAL: Faculdade de Medicina - FAMED - Barbalha
TÍTULO:

IMPACT OF QUERCETIN ON OXIDATIVE STRESS AND MITOCHONDRIAL HOMEOSTASIS DURING CARDIAC HYPERTROPHY

 

PALAVRAS-CHAVES:

Mitochondria. Cardiac hypertrophy. Quercetin. Reactive oxygen species.

PÁGINAS: 63
GRANDE ÁREA: Ciências Biológicas
ÁREA: Bioquímica
RESUMO:

Oxidative stress, characterized by the accumulation of reactive oxygen species (ROS), is implicated in the pathogenesis of several diseases, including cardiac hypertrophy. Although ROS are essentials for several physiological processes, excessive amounts may damage cardiomyocyte components, compromising their function and thus triggering a number of adverse changes such as cardiac fibrosis, impaired contraction, cell death by necrosis and apoptosis. The mitochondrial electron transport chain (ETC) is a known source of ROS. Because mitochondria account for about 25% of the mass of cardiomyocytes, they are considered one of the most significant sources of ROS in the heart. Thus, mitochondria have been the target of several studies using cardiac hypertrophy models. The flavonoid quercetin, is a potent ROS scavenger and having several beneficial effects on the cardiovascular system, including antihypertrophic effects. In this work, we tested whether quercetin could attenuate the cardiac hypertrophy by improving the redox balance and mitochondrial homeostasis. To this hypothesis we treated mice with intraperitoneal injections of isoproterenol (30 mg/kg/day) for 4 consecutive days. On the fifth day, some of these animals were euthanized and the remaining mice were relocated to two subgroups. From that point on, one group received only isoproterenol (ISO group) (30 mg/kg/dia) and another group received isoproterenol and quercetin (ISO+QUE group) orally (10 mg/kg/day) for 4 more days. The animals treated with ISO for 4 days showed increased cardiac weight/tibia length ratio, increased total protein content, decreased sulfhydryl protein content, compromised antioxidant enzyme activity and high H₂O₂ production. Intervention with quercetin treatment from this point on was able to attenuate cardiac hypertrophy, reestablish sulfhydryl protein levels and antioxidant activity, in addition to effectively blocking the H₂O₂ production. In addition, we observed that isoproterenol hypertrophic stimulation decreases mitochondrial superoxide dismutase (MnSOD) expression and activity, while quercetin reverses this effect. Quercetin also protects mitochondria against opening of mitochondrial permeability transition pore (mPTP) in vivo and in vitro. Taken together, these results show that quercetin is able to attenuate isoproterenol-induced cardiac hypertrophy by improving mitochondrial function and redox balance.

MEMBROS DA BANCA:
Externo à Instituição - CLAUDENER SOUZA TEIXEIRA - UFMA
Presidente - 1364396 - HEBERTY DI TARSO FERNANDES FACUNDO
Externo à Instituição - JOSÉ GALBERTO MARTINS DA COSTA - URCA
Interno - 1305746 - THIAGO MIELLE BRITO FERREIRA OLIVEIRA