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

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. Hyperglycemia 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 as free fatty acids and leptin, also contribute to increased reactive oxygen species (ROS). The major roles of GSH (γ-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 on the concentration of total glutathione (GSH) in Hep G2 cells and 2) to determine whether this flavonoid could protect the cells against glucose-induced oxidative stress. Hep G2 cells was supplemented with 0.5µM and 1.0µM of myricetin for 4 hours or 0.5µM and 1.0µM of myricetin plus 20µM 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 0.5µM of myricetin for 4 hours at 37° 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 at low concentration (0.5µM) protects Hep G2 cells against glucose toxicity affecting the glutathione level.