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

OBJECTIVE: To investigate the role and mechanism of protein kinase N2 (PKN2) in hydrogen peroxide (H(2)O(2))-induced injury of PC12 cells. METHOD: s. PC12 cells were transfected with lentivirus to knock down or overexpress PKN2 and then were treated with 300 μM H(2)O(2) 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: H(2)O(2) treatment could significantly reduce PC12 cell viability and promote cell apoptosis and oxidative stress. PKN2 overexpression inhibited H(2)O(2)-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 H(2)O(2)-induced oxidative stress injury and apoptosis in PC12 cells by activating the mTOR pathway.