Efeito do treinamento resistido sobre a atividade enzimática da MMP-2 e antioxidantes no ventrículo esquerdo de ratos obesos

Detalhes bibliográficos
Ano de defesa: 2013
Autor(a) principal: Lino, Anderson Diogo de Souza
Orientador(a): Duarte, Ana Cláudia Garcia de Oliveira lattes
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de São Carlos
Programa de Pós-Graduação: Programa Interinstitucional de Pós-Graduação em Ciências Fisiológicas - PIPGCF
Departamento: Não Informado pela instituição
País: BR
Palavras-chave em Português:
Palavras-chave em Inglês:
Área do conhecimento CNPq:
Link de acesso: https://repositorio.ufscar.br/handle/20.500.14289/1350
Resumo: Obesity is associated with increased lipid peroxidation in the myocardium and an increased susceptibility to oxidative damage, which can lead to several cardiovascular risk factors including heart failure, insulin resistance, hypertension and dyslipidemia. The ONOOin conjunction with normal intracellular levels of reduced glutathione (GSH), are responsible, among other factors, to activate the matrix metalloproteinases (MMPs) that are important in mediating the deleterious effects of cardiovascular diseases. The unregulated activity of MMPs, such as MMP-2, may promote the development of heart disease. Resistance training (RT) can mitigate or even reverse the obesity, prevent against lipid peroxidation, increasing the levels of antioxidant enzymes, improved lipid profile, reduced cardiovascular risk and reduce the concentration of fibrosis and dysregulation of MMP-2. Purpose: To analyze the effects of RT high intensity on ladder associated with high fat diet on the activity of MMP-2 and antioxidant enzymes (SOD Total, Mn-SOD, CAT, GPx), GSH and lipid peroxidation, related to left ventricle remodeling in rats. Methods: 60 rats Wistar were used in this study, which was divided into three phases: 1) three week period of obesity induction, control group fed with standard diet (CT-S n = 30) and control group fed with high fat diet (CT-H n = 30); 2) effect of fat diet for eight weeks, sedentary standard diet group (SED-S n = 10) and high fat diet sedentary (SED-H n = 10), 3) effect of high-intensity RT on ladder for eight weeks associated with high-fat diet, RT standard diet (RT-S n = 10) and RT high-fat diet RT (RT-H n = 10). Results: The three-week obesity induction was effective in promoting the group CTH increased body mass (p <0.05), LV mass (p <0.05) and activity of MMP-2 (p <.001), TBRs (p <0.03) and decrease the citrate synthase activity (p <0.05). After eight weeks of high fat diet, the SED-H group had a higher body mass (p <0.02) compared to SED-S. The volume LV for SED-H group was higher compared to that of CT-H (p <0.001), but did not change when compared to SED-S. There was a lower activity of MMP-2 (p <0.05) in SED-S compared to CT-H. Lipid accumulation was observed (p <0.007) in the LV of SED-H group compared to CT-H. The longer life associated with high-fat diet promoted suppression in the enzymatic activity of SOD Total (p <0.01) and Mn-SOD (p <0.002) (SED-H), and increased activity of GSH (p <0.004). The RT was effective in attenuating the gain body mass in RT-H group compared to SED-H, even though higher compared to RT-S (p <0.005). In the group RT-H of MMP-2 activity was higher (p <0.03) compared to RT-S, but lower (p <0.04) compared to SED-H. The RT promoted greater citrate synthase activity (p <0.03), SOD Total (p <0.001) and Mn-SOD (p <0.03) and lower activity of GSH (p <0.01) in RT-H. There was no significant increase in TBARs level in the VE of the RT-H group. However, we observed increased lipid content (p <0.04). Conclusion: We conclude that high intensity RT, in obese rats, could be a pharmacological tool able to positively modulate the activity of MMP-2 and some antioxidant enzymes such as SOD Total, Mn-SOD and GSH. These effects are important for the maintenance of heart health, relieving the deleterious effects on obesityrelated of the left ventricle remodeling, so experiment.