Apoptose em tecido cardíaco e estresse
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Data
2012-04-24
Autores
Conrado, Ricardo de Moura [UNIFESP]
Orientadores
Spadari, Regina Celia [UNIFESP]
Tipo
Dissertação de mestrado
Título da Revista
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Resumo
A reação de estresse caracteriza-se por elevada atividade adrenérgica e
glicocorticóide. Estes mediadores químicos modulam a atividade e o remodelamento
cardíacos, do qual a apoptose é um dos mecanismos. O objetivo deste trabalho é
analisar processos adaptativos induzidos por estresse relacionados à apoptose em tecido
cardíaco. Ratos machos, adultos foram submetidos a três sessões de choque nas patas
(1.0 mA, 1 s, 5-25 s intervalo entre os pulsos) com 30 min de duração e ou tratados com
mifepristona (3,7 mg/Kg, ip) dois dias antes e nos dias em que foram submetidos o
estresse. Após o sacrifício, o coração foi isolado e processado para análise histológica,
imunoistoquímica das proteínas p53, bcl-2 e bax, e ensaio do cometa. Os resultados
obtidos mostram que: (1) estresse por choque nas patas induz danos ao DNA em
cardiomiócitos, com aumento da expressão das proteínas p53 e bax; (2) o bloqueio dos
receptores de glicocorticóide e progesterona por mifepristona também induz danos ao
DNA e aumento da expressão da proteína pró-apoptótica bax. Estes efeitos são
potencializados pelo estresse. Mifepristona também reduz a expressão da proteína p53.
Conclui-se que os glicocorticóides exercem papel protetor contra apoptose em tecido
cardíaco, principalmente durante situações de estresse. A participação de outros
mecanismos além daqueles relacionados aos glicocorticóides nos processos
desencadeados por estresse merece ser investigada.
The stress reaction is characterized by high adrenergic and glucocorticoid activity. These chemical mediators modulate the heart functioning and remodeling, including cardiomyocytes apoptosis. The aim of this work is to analyse the stress induced adaptive processes related to apoptosis in cardiac tissue. Male adult rats were submitted to three sessions of footshock stress (1.0 mA, 1 s, 5-25 interval), 30 min duration, and/or treated with mifepristone (3.7 mg/Kg, ip) two days before and in the days of footshock stress. The rats were euthanized and the heart was prepared for histological analysis, immunohistochemistry for p53, bcl-2 and bax proteins, and for the comet assay. The results have shown that: (1) footshock stress caused DNA damage in cardiomyocytes, with increased p53 and bax expression; (2) the blockade of glucocorticoids and progesterone receptors with mifepristone also induced DNA damage and enhanced bax expression. These effects were potentiated by stress. Moreover, the expression of p53 is reduced by mifepristone associated or not to stress. It is concluded that glucocorticoids play a protective role against apoptosis in the cardiac tissue, mostly during stress. Other mechanisms induced by stress related to the processes here analysed need to be investigated.
The stress reaction is characterized by high adrenergic and glucocorticoid activity. These chemical mediators modulate the heart functioning and remodeling, including cardiomyocytes apoptosis. The aim of this work is to analyse the stress induced adaptive processes related to apoptosis in cardiac tissue. Male adult rats were submitted to three sessions of footshock stress (1.0 mA, 1 s, 5-25 interval), 30 min duration, and/or treated with mifepristone (3.7 mg/Kg, ip) two days before and in the days of footshock stress. The rats were euthanized and the heart was prepared for histological analysis, immunohistochemistry for p53, bcl-2 and bax proteins, and for the comet assay. The results have shown that: (1) footshock stress caused DNA damage in cardiomyocytes, with increased p53 and bax expression; (2) the blockade of glucocorticoids and progesterone receptors with mifepristone also induced DNA damage and enhanced bax expression. These effects were potentiated by stress. Moreover, the expression of p53 is reduced by mifepristone associated or not to stress. It is concluded that glucocorticoids play a protective role against apoptosis in the cardiac tissue, mostly during stress. Other mechanisms induced by stress related to the processes here analysed need to be investigated.
Descrição
Citação
CONRADO, Ricardo de Moura. Apoptose em tecido cardíaco e estresse. 2012. 42f. Dissertação (Mestrado) - Instituto de Saúde e Sociedade, Universidade Federal de São Paulo, Santos, 2012.