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. 2021 Dec 16;12:797298. doi: 10.3389/fphar.2021.797298

TABLE 1.

Comprehensive information about the effects of myricetin in in vivo and in vitro models cerebral ischemia.

Pharmacological effect Object Drug administration Possible mechanisms References
*Reduce neuronal apoptosis Rat *5, 25 mg/kg *Suppress pro-inflammatory cytokine, MDA, and reactive oxygen species production Sun et al. (2018)
*Reduce infarct area *improve neurological deficits *i.g *Increase GSH production and SOD and Akt activity
*Once daily, 7 days *Decrease NF-κB activity
*Reduce neuronal loss and apoptosis Rat *10, 20 mg/kg *Reduce MDA and reactive oxygen species production Wu et al. (2016)
*Reduce infarct area *i.g *Increase Nrf2 function
*Improve neurological deficits *2 h before and every day after MCAO *Improve mitochondrial function
*Improve learning and memory function
Attenuate OGD-induced neuronal damage, reactive oxygen species production, and mitochondrial depolarization SH-SY5Y cells *10 nM *Inhibit caspase-3 activity Wu et al. (2016)
*3 h before ODG exposure
Prevent glutamate-induced nuclear fragmentation and cell death Rat cortical neurons *0.1, 0.3, 1, 3, 10 μM Suppress Ca2+ overloading, reactive oxygen species production, and caspase-3 activation Shimmyo et al., 2008
*24 h of pretreatment along with 24 h of simultaneous treatment
Reduce 4-AP-induced Ca2+ influx, neuronal depolarization, and glutamate release Isolated nerve terminals 30 μM co-incubation Block the N-type and P/Q-type Ca2+ channel Chang et al. (2015)
*Reduce OGD/R-induced pro-inflammatory cytokine production and decrease in eNOS expression/phosphorylation/activity, BH4/BH2 ratio, and GSH levels HBMECs *10, 30, 60 μM Activate the Akt and Nrf2 signal Zhang et al. (2019)
*Pretreatment, 24 h