Insulin exerts neuroprotective effects via Akt/Bcl-2 signaling pathways in differentiated SH-SY5Y cells

Abstract

In the present study, the changes in the cell viability at different concentrations of hydrogen peroxide (H₂O₂) for 3 h used to establish a model of oxidative stress. Further assays with 200 μM H₂O₂ induces significant changes in the levels of lactate dehydrogenase (LDH), nitric oxide (NO), reactive oxygen species (ROS) and calcium ion (Ca²⁺) in neuronal cells, but insulin can effectively diminish the oxidative damages. Moreover, cells treated with insulin increased the H₂O₂-induced suppression of glutathione levels and exerted an apparent suppressive effect on oxidative products. The results of Akt, Bcl-2, Bax, IRβ, IGF-1Rβ, IRS-1 and IRS-2 showed that insulin treatment had a protective effect on H₂O₂-induced oxidative stress in RA-differentiated SH-SY5Y neuroblastoma cells.

• Insulin
• insulin receptors
• insulin receptor substrates
• neurons
• reactive oxygen species
• SH-SY5Y

Declaration of interest

The authors have no conflicts of interest to declare. This work was supported by a post-doctoral fellowship grant from Kyung Hee University in 2011–2013 (KHU-20110696).