Glutaredoxin 1 protects neurons from oxygen-glucose deprivation/reoxygenation (OGD/R)-induced apoptosis and oxidative stress via the modulation of GSK-3β/Nrf2 signaling.

摘要: Increasing evidence has indicated that glutaredoxin 1 (GRX1) is a potent antioxidant protein promotes cell survival under conditions of oxidative stress. Oxidative stress-induced neuronal injury contributes to cerebral ischemia/reperfusion injury. However, the role GRX1-mediated defense against damage during not been thoroughly investigated. Thus, objective this study was evaluate whether GRX1 protects neurons oxygen-glucose deprivation/reoxygenation (OGD/R)-evoked stress in an vitro model Our data revealed induced by OGD/R treatment neurons. Functional assays loss exacerbated OGD/R-induced apoptosis and generation reactive oxygen species (ROS), while up-regulation protected OGD/R-evoked Further investigation promoted nuclear expression factor erythroid 2-related 2 (Nrf2) enhanced transcription Nrf2/antioxidant response element (ARE) GOD/R-exposed Furthermore, activation Nrf2/ARE associated with modulation glycogen synthase kinase-3β (GSK-3β). GSK-3β inhibition blocked knockdown-mediated suppression Nrf2 activation. Notably, partially reversed anti-oxidative OGD/R-exposed In summary, these findings indicate enhancing via GSK-3β. suggests potential neuroprotective