Protein Kinase N2 Reduces Hydrogen Peroxide-inducedDamage and Apoptosis in PC12 Cells by AntiOxidative Stress and Activation of the mTOR Pathway

Abstract

Objective. To investigate the role and mechanism of protein kinase N2 (PKN2) in hydrogen peroxide (H2O2)-induced injury of PC12 cells. Methods. PC12 cells were transfected with lentivirus to knock down or overexpress PKN2 and then were treated with 300 μM H2O2 to establish a cell model of oxidative stress injury. The cell viability of PC12 cells in each group was determined by the CCK-8 method. Biochemical assays were used to measure reactive oxygen species (ROS), malondialdehyde (MDA) levels, and superoxide dismutase (SOD) activity. Western blot was used to detect the protein expressions of PKN2, caspase-3, cleaved-caspase-3, PARP, cleaved-PARP, p-mTOR, and mTOR in PC12 cells in each group. Results. H2O2 treatment could significantly reduce PC12 cell viability and promote cell apoptosis and oxidative stress. PKN2 overexpression inhibited H2O2-induced apoptosis and oxidation damage by increasing PC12 cell viability, SOD activity, and p-mTOR protein expression, reducing intracellular ROS and MDA levels, and cleaved-caspase-3 and cleaved-PARP protein expression. Conclusion. PKN2 overexpression can alleviate H2O2-induced oxidative stress injury and apoptosis in PC12 cells by activating the mTOR pathway.