Downregulation of FOXO4 promotes neuronal survival by mediating oxidative-stress–induced apoptosis after cerebral ischemia/reperfusion injury

Purpose: To investigate the effect of FOXO4 on cerebral ischemia/reperfusion (CIR) injury and underlying mechanism.Methods: An in vitro (IR) model was achieved using oxygen-glucose deprivation/reoxygenation (OGD/R). Expression RNA protein determined quantitative real time polymerase chain reaction (qRT-PCR) western blotting, respectively. Cell viability apoptosis were MTT assay flow cytometry, Commercial kits used to measure lactate dehydrogenase (LDH), reactive oxygen species (ROS), chloramphenicol acetyltransferase (CAT), malondialdehyde (MDA), superoxide dismutase (SOD).Results: Following OGD/R, mRNA expressions upregulated SH-SY5H human neuroblastoma cells. ODG/R reduced cell proliferation increased proportion apoptotic cells, these effects inhibited by knockdown (p < 0.05). Levels cleaved caspase 3 poly(ADP-ribose) polymerases (PARPs) after increaseswere knockdown. ROS content levels LDH MDA decreased CAT SOD ODG/R, this reduction reversed 0.05).Conclusion: The results demonstrate that promotes inhibits cellular via oxidative stress CIR injury, indicating a new therapeutic target for treatment injury.
 Keywords: FOXO4, Neuronal survival, Oxidative stress, Cerebral