Myricitrin (Myricitrine), a flavonoid compound isolated from the root bark of Myrica cerifera, exerts antinociceptive effects.

In mice, Myricitrin (10/30 mg/kg, i.p.) blocks apomorphine-induced stereotypy and climbing behaviors, while also prolonging the hindlimb withdrawal time.

In rodent models of chemical and mechanical pain, Flurbiprofen activates protein kinase Cα and PKCε, while Myricitrin blocks this action, thereby exerting a significant analgesic effect. The pain-relief mechanism of Myricitrin is attributed to a decrease in calcium ion influx and the opening of voltage-dependent and small-conductance calcium-activated potassium (K+) channels. Additionally, Myricitrin inhibits the expression of the p53 gene, which leads to the activation of caspase-3 and the MAPK signaling pathway, while altering the expression pattern of anti-apoptotic and pro-apoptotic genes. Consequently, this reduces H₂O₂-induced apoptosis in vascular endothelial cells.