Overall, these results demonstrated that miR-152-3p protected neurons from OGD/R-induced apoptosis and ROS production by reinforcing Nrf2/ARE antioxidant signaling through targeting and inhibiting PSD-93, findings that suggest miR-152-3p is a potential target for neuroprotection during ischemic stroke.
In vitro, oxygen and glucose deprivation/reperfusion (OGD/R)-induced ischemic stroke in BV-2 microglia and primary neurons, and bEnd.3 mouse cerebral microvascular endothelial cells (ECs) were also used.
Together, our data revealed possible participation of lncRNAs in the pathophysiology of OGD/R and thereby provided new insights into the studies of potential therapeutic targets for ischemic stroke.
Primary rat neural cells were exposed to PACAP-27 or PACAP-38 before induction of experimental acute ischemic stroke via oxygen-glucose deprivation-reperfusion (OGD/R) injury.
We used the middle cerebral artery occlusion (MCAO) rat model as well as oxygen and glucose deprivation-reoxygenation (OGD/R) endothelial cells as ischemic stroke models to investigate the efficacy and mechanisms of treating ischemic stroke with the combination of GBC and TH.
In this study, we used oxygen/glucose deprivation and reperfusion (OGD/R) condition to mimic an ischemic stroke <i>in vitro.</i> Matrix metalloproteinases (MMP) activity was measured in endothelial cell media.