O Papel da metformina no controle do estresse oxidativo em músculo de ratos diabéticos

Abstract

CHAPTER II: Introduction and Objectives: Metformin can act in muscle inhibiting the complex I of the electron transport chain and activating a signaling cascade for glut-4 translocation to the membrane cell. Our hypothesis is that this inhibition can decrease mitochondrial reactive oxigen species (ROS), minimizing cell damage caused by oxidative stress. Thus, the aim of this study was to evaluate the activity and expression of oxidative stress enzymes, total antioxidant status and lipid peroxidation in gastrocnemius muscle of rat with induced diabetic Mellitus and treated with metformin. Materials and Methods: The DM was induced in Wistar rats divided into four groups: untreated, treated with insulin, insulin plus metformin, and metformin. A non-diabetic group was used as control. The gastrocnemius muscle was collected and homogenized to evaluate the following parameters: superoxide dismutase (SOD) and catalase (activity and immunoblotting), glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase (activity), reduced glutathione, lipid peroxidation and total antioxidant capacity were measured. Results and conclusions: he group treated with metformin showed prevention in increased activity and expression of SOD and catalase, and kept the total antioxidant capacity and G6PDH activity when compared to the untreated group. These results seem to be related to lower lipid peroxidation. Therefore, this study suggest that metformin may is involved in the regulation of the oxidative stress in muscle cells decreasing lipid peroxidation which could improve glucose uptake.