Protective effect of the flavonoid myricetin on glucose induced oxidative stress in Hep G2 cells

Abstract

Myricetin is a naturally occurring flavonol with hydroxyl substitutions at the 3, 5, 7, 3, , 4, and 5, positions and has a hypoglycaemic and hypotrigyceridemic effect in diabetes mellitus. Hyperglicemia in diabetes can induce oxidative stress via several mechanisms. These include glucose autoxidation, the formation of advanced glycation end-products (AGE), and activation of the polyol pathway. Other circulating factors such free fatty acids and leptin, also contribute to increased reactive oxygen species (ROS). The major roles of GSH ( -glutamiylcysteinylglycine) are to maintain the intracellular redox balance and to eliminate ROS in cells. The aims of this study were 1) to investigate the effect of the flavonoid myricetin (Sigma) on the concentration of total glutathione (GSH) in Hep G2 cells and 2) to determine whether this flavonoid could protect thi cells against glucose-induced oxidative stress. Hep G2 cells was supplemented with with 0.5  M and 1.0  M of myricetin for 4 hours or 0.5  M and 1.0  M of myricetin plus 20  M glucose for same time. Concentration of GSH in cells was determined by Cayman, s GSH assay kit with enzymatic recycling method, using glutathione reductase. Exposure the Hep G2 cells to 0.5  M of myricetin for 4 hours at 37 degrees C resulted in significant increased of the GSH level (p 0.05) when compared with control cells. This data suggest that major features of glucose-induced hepatotoxicity are partially mediated by oxidative stress, and that myricetin in low concentration (0.5  M) protect Hep G2 cells against glucose toxicity affecting the glutathione level.