Akt enhances nerve growth factor-induced axon growth via activating the Nrf2/ARE pathway.

Spinal cord injury (SCI) leads to the loss of structure and function of axons. However, injured axons cannot grow or regenerate spontaneously following injury. Generally, only when treated with neurotrophins, such as nerve growth factor (NGF), will the neurons sprout new axons. Akt is one of the central kinases of neurocytes. PC12 cells are a frequently used cell model for neural differentiation and development studies. The nuclear factor erythroid 2‑related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway is a main mechanism in prevention from oxidative stress, which may damage the nervous system. The present study employed this cell model to investigate whether Akt could induce axon growth in PC12 cells on the basis of NGF treatments. The results showed that Akt overexpression significantly increased cell proliferation and decreased cell apoptosis. Additionally, Akt overexpression activated Nrf2/ARE pathways. In conclusion, the experiments indicated that Akt overexpression contributed to axon regeneration induced by NGF in PC12 cells through activating the Nrf2/ARE pathway.