CHIP Overexpression Prevents Both AKT Phosphorylation in Serine 473 and eIF2α Phosphorylation in Serine 51 Induced by Global Brain Ischemia, Followed by 3 hr of Reperfusion in the Hippocampus
(A) Left: western blots for p-AKT (Ser473) and total AKT of whole hippocampus homogenates under different experimental conditions. Right: quantification of normalized optical density for p-AKT and total AKT bands. (B) Left: western blots for p-eIF2α (Ser51) and total eIF2α of whole hippocampus homogenates under different experimental conditions. Right: quantification of normalized optical density for p-eIF2α and total eIF2α bands. β-actin was used as a loading control. n = 4 animals per group; 95% confidence interval (CI); *p < 0.05; **p < 0.01; NS, non-significant. Error bars indicate ± SEM. S, sham operated; GBI, global brain ischemia followed by 3 hr of reperfusion; GFP+GBI, rAAV8-733-GFP infected + GBI; CHIP+GBI, rAAV8-733-CHIP infected + GBI.