Myricetin Prevents Cataract Formation by Inhibiting the Apoptotic Cell Death Mediated Cataractogenesis

BACKGROUND The current research work aimed to explore the protective role of myricetin against cataractogenesis in humans, in terms of its anti-apoptotic potential. MATERIAL AND METHODS Human eye lens epithelial cells were exposed to oxidative stress by treating with hydrogen peroxide (H₂O₂). The levels of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) were determined using standard detection kits. DAPI (4',6-diamidino-2-phenylindole), AO/EB (acridine orange/ethidium bromide) and Annexin V/propidium iodide (PI) staining assays were used for the assessment of cell apoptosis. Western blotting was used to examine the protein concentrations. RESULTS The exposure of human epithelial eye lens cells to H₂O₂ led to significant accumulation of reactive oxygen species molecules. Treatment of the H₂O₂-stressed epithelial cells with myricetin caused significant (P<0.05) increased levels of SOD, CAT, and GSH. Western blot analysis also showed a significant (P<0.05) increase in the expression of SOD, CAT, and GSH levels in human epithelial eye lens cells. Additionally, myricetin administration to H₂O₂-treated epithelial eye lens cells caused a significant decline in cell apoptosis ratio. The induction of apoptosis was associated with upregulation of Bax and downregulation of Bcl-2. CONCLUSIONS The results of this study showed the potential of myricetin in protecting the apoptosis driven cataract formation in humans.