*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 |