The Effects of Diabetes Induction on the Rat Heart: Differences in Oxidative Stress, Inflammatory Cells, and Fibrosis between Subendocardial and Interstitial Myocardial Areas

Autor(es)

Guido, Maria C. ; Marques, Alyne F. ; Tavares, Elaine R. ; Tavares de Melo, Marcelo D. ; Salemi, Vera M. C. ; Maranhao, Raul C.

• Tipo de documento: Artigo Científico
• Fonte: OXIDATIVE MEDICINE AND CELLULAR LONGEVITY; v. 2017, p. 11-pg., 2017-01-01.

Resumo

Diabetic cardiomyopathy (DCM) is characterized by cardiac remodeling and impaired diastolic function that may lead to heart failure. The aim of this study was to evaluate oxidative stress, inflammatory cells, and fibrosis in both subendocardial (SEN) and interstitial (INT) areas of the myocardium. Male Wistar rats were allocated to 2 groups of 9 animals, a control (CT) group and streptozotocin-induced diabetes (DM). After 8 weeks, echocardiography morphometry, protein expression, and confocal microscopy in SEN and INT areas of the left ventricle (LV) were performed. The echocardiographic analysis showed that diabetes induction leads to cardiac dilation, hypertrophy, and LV diastolic dysfunction. As compared to CT, the induction of diabetes increased inflammatory cells and fibrosis in both SEN and INT areas of DM myocardium and increased ROS generation only in SEN. Comparing the SEN and INT areas in the DM group, inflammatory cells and fibrosis in SEN were greater than in INT. In conclusion, diabetic myocardium SEN area, wherein oxidative stress was more pronounced, is more susceptible to cardiac dysfunction than INT area. This finding can be important for the understanding of the heart remodeling process occurring in DCM and perhaps to engender targeted therapies to attenuate or revert DCM-related diastolic dysfunction. (AU)

• Processo FAPESP: 14/03742-0 - Projeto temático em medicina translacional: nanopartículas que se ligam a receptores de lipoproteínas no tratamento da aterosclerose, do infarto agudo de miocárdio, do pós-transplante de coração, do câncer e da endometriose
• Beneficiário: Raul Cavalcante Maranhao
• Modalidade de apoio: Auxílio à Pesquisa - Temático