Banca de DEFESA: CICERA ÉDNA BARBOSA DAVID

Uma banca de DEFESA de MESTRADO foi cadastrada pelo programa.
DISCENTE : CICERA ÉDNA BARBOSA DAVID
DATA : 04/02/2019
HORA: 14:00
LOCAL: Faculdade de Medicina - FAMED - Barbalha
TÍTULO:

Impact of Calorie Restriction on Oxidative Stress and  mitochondrial ATP sensitive potassium channel During cardiac hypertrophy in mice 

PALAVRAS-CHAVES:

Cardiac hypertrophy. Caloric Restriction. Mitochondrion. Reactive Oxigen Species. Mitochondrial ATP-sensitive K+ channel.

PÁGINAS: 72
GRANDE ÁREA: Ciências Biológicas
ÁREA: Bioquímica
SUBÁREA: Metabolismo e Bioenergética
RESUMO:

Cardiac hypertrophy is a compensatory response of the heart to an increase in blood pressure or volume. Although it is a temporary beneficial response, it often leads to hypertrophic cardiomyopathy and congestive heart failure. Caloric restriction (CR) is a powerful intervention to improve health and delay of aging, its effects involve improve-ment in energy metabolism and oxidative stress, in which mitochondria play a central role. Mitochondria have an ATP-sensitive K+ channels (mitoKATP), whose opening leads to cellular protection through mechanisms related to the reduction of cellular oxidative stress. This paper investigated the role of CR in the prevention of isoproterenol-induced cardiac hypertrophy in vivo by preventing the production of reactive oxygen species and maintaining antioxidant activity. Additionally, we investigated the involvement of mi-toKATP in cardiac hypertrophy. In order to establish a protocol for induction of caloric restriction in mice, we counted (in grams) the standard diet consumption of Swiss mice for 2 weeks. After this period the animals were randomly divided into two groups: ad libitum (AL group) and fed with 60% of the average calorie intake (RC group - calculated as above) for an additional 4 weeks. To induce cardiac hypertrophy, mice were treated with isoproterenol (ISO) (30 mg / kg / day) for 8 days. For inhibition of mitoKATP, bloc-kers, 5-hydroxydecanoate (5-HD) (10 mg / kg / day) and glybenclamide (GLI) (6 mg / kg / day) were used from the 5th day. Isoproterenol-treated mice had elevated heart weight/tibia length ratios and cardiac protein levels. These gross hypertrophic markers were significantly reduced in CR mice. Cardiac tissue from isoproterenol-treated CR mice also produced less H2O2 and had lower protein sulfydryl oxidation. Additionally, calorie restriction blocked hypertrophic-induced antioxidant enzyme (catalase, superoxide dis-mutase and glutathione peroxidase) activity repression during cardiac hypertrophy. Re-markably, mitoKATP activity has been shown to be repressed in isolated mitochondria from hypertrophic hearts, in a manner sensitive to CR. Finally, as evidence of the princi-ple of mitoKATP involvement in protection against hypertrophy we found that pharmaco-logical inhibition of mitoKATP (using 5-HD and GLI) significantly blocked the protective effects of CR. Together these data suggest that CR improves redox balance during car-diac hypertrophy, and performs this process in a mechanism involving mitoKATP activation.

MEMBROS DA BANCA:
Interno - 2353800 - CLAUDIO GLEIDISTON LIMA DA SILVA
Interno - 2185176 - FRANCISCO NASCIMENTO PEREIRA JUNIOR
Presidente - 1364396 - HEBERTY DI TARSO FERNANDES FACUNDO
Externo à Instituição - HENRIQUE DOUGLAS MELO COUTINHO - URCA
Externo à Instituição - IRWIN ROSE ALENCAR DE MENEZES - URCA