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

J Recept Signal Transduct Res. 2015 Feb;35(1):1-7. doi: 10.3109/10799893.2014.922576. Epub 2014 May 22.

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 (Ca(2+)) 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.

Keywords: Insulin; SH-SY5Y; insulin receptor substrates; insulin receptors; neurons; reactive oxygen species.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • Calcium / metabolism
  • Cell Differentiation / drug effects
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Humans
  • Hydrogen Peroxide / toxicity
  • Insulin / administration & dosage*
  • Insulin / metabolism
  • Neuroblastoma / metabolism
  • Neurons / drug effects*
  • Neurons / pathology
  • Neuroprotective Agents / administration & dosage*
  • Oxidative Stress / drug effects*
  • Reactive Oxygen Species / metabolism
  • Signal Transduction / drug effects
  • Tretinoin / administration & dosage

Substances

  • Insulin
  • Neuroprotective Agents
  • Reactive Oxygen Species
  • Tretinoin
  • Hydrogen Peroxide
  • Calcium