FIGURE 2.

Neuroprotective effects and possible mechanisms of myricetin in models of cerebral ischemia. Myricetin inhibits (i) OGD/R-induced inflammation, decrease in eNOS expression, phosphorylation, and activity, decrease in intracellular BH4/BH2 ratio, and decrease in intracellular GSH levels in endothelial cells via stimulation of Akt and Nrf2, (ii) glutamate-induced nuclear fragmentation and cell death in primary cultured rat cortical neurons via suppression of Ca²⁺ overloading, and (iii) OGD-induced neuronal damage, reactive oxygen species production, and mitochondrial depolarization in SH-SY5Y cells via inhibition of caspase-3. Myricetin administration can also reduce neuronal apoptosis and infarct area and improve neurological deficits in a rat model of MCAO via increasing Akt activity, decreasing p38 and NF-κB activity, and increasing Nrf2 nuclear translocation.