Profile of pterostilbene-induced redox homeostasis modulation in cardiac myoblasts and heart tissue

• Autor(a) principal: Couto, Gabriela Klein
• Data de Publicação: 2018
• Outros Autores: Fernandes, Rafael Oliveira, Lacerda, Denise dos Santos, Carraro, Cristina Campos, Turck, Patrick, Bianchi, Sara Elis, Ferreira, Gustavo Dias, Brum, Ilma Simoni, Bassani, Valquiria Linck, Belló-Klein, Adriane, Araújo, Alex Sander da Rosa
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRGS
• Texto Completo: http://hdl.handle.net/10183/188330
• topic: Homeostase; Estresse oxidativo; Cardiopatias; Mioblastos cardíacos; Antioxidant enzymes; Cardiac myoblasts; Cardiac tissue; Cyclodextrin; H9c2 cells; Oxidative damage; Oxidative stress; Pterostilbene

This study was designed to investigate the effect of pterostilbene (PTS) on cardiac oxidative stress in vitro, as this is a simple and promising methodology to study cardiac disease. Cardiac myoblasts (H9c2 cells) and homogenised cardiac tissue were incubated with the PTS and cyclodextrin (PTS ? HPbCD) complex for 1 and 24 h, respectively, at concentrations of 50 lM for the cells and 25 and 50 lM for cardiac tissue. The PTS ? HPbCD complex was used to increase the solubility of PTS in water. After the pretreatment period, cardiomyoblasts were challenged with hydrogen peroxide (6.67 lM) for 10 min, while cardiac tissue was submitted to a hydroxyl radical generator system (30 min). Cellular viability, oxidative stress biomarkers (e.g. total reactive oxygen species (ROS), carbonyl assay and lipoperoxidation) and the antioxidant response (e.g. sulfhydryl and the antioxidant enzyme activities of superoxide dismutase, catalase and glutathione peroxidase) were evaluated. In cardiomyoblasts, the PTS ? HPbCD complex (50 lM) increased cellular viability. Moreover, the PTS ? HPbCD complex also significantly increased sulfhydryl levels in the cells submitted to an oxidative challenge. In cardiac tissue, lipid peroxidation, carbonyls and ROS levels were significantly increased in the groups submitted to oxidative damage, while the PTS ? HPbCD complex significantly reduced ROS levels in these groups. In addition, the PTS ? HPbCD complex also provoked increased catalase activity in both experimental protocols. These data suggest that the PTS ? HPbCD complex may play a cardioprotective role through a reduction of ROS levels associated with an improved antioxidant response.