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Myricetin-flavonol prevents D-glucose induced dysfunction and oxidative stress in Hep G2 cells

Myricetin is a naturally occurring flavonol with hydroxyl substitutions, and was found to be effective in scavenging radicals generated by both enzymatic and nonenzymatic systems. An imbalance in the antioxidant protective mechanism leading to oxidative stress in the cells is being identified as a common factor in diabetes mellitus and several other disorders. Free radicals are formed disproportionately in diabetes by glucose oxidation, nonenzymatic glycation of proteins, and the subsequent oxidative degradation of glycated proteins. The aims of this study were: 1) to investigate the effect of the low concentration range of myricetin on cell viability and activity of lactate dehydogenase (LDH) - as indicator of cell damage and 2) investigate activities of endogenous antioxidative enzymes: glutathione peroxidase (GPx) and glutathione reductase (GR). GPx catalyzes the reduction of hydroperoxides, including hydrogen peroxide, by reduced glutathione and functions to protect the cell from oxidative damage. Hep G2 cells were supplemented with various concentrations of myricetin (10-5M, 10-7M, 10-9M) for 24 h in hyperglicemic conditions (20 mM glucose). Cell viability was assessed by MTT test and GPx and GR activity were determined using Cayman, s Assay Kit. Exposure Hep G2 cells to 20 mM glucose during 24 h resulted in significantly decrease in GPx activity (p 0.05). Myricetin in concentration of 10-9M significantly enhanced GPx activity in Hep G2 cells but didn, t effect on GR activities. Results of the MTT assay showed that myricetin in all low concentrations range significantly enhance viability of the Hep G2 cells. Concluding, this study shows that myricetin in low concentration range protected Hep G2 cells against D-glucose induced dysfunction and oxidative stress.

Myricetin; diabetes; oxidative stress; Hep G2 cells

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