Insulin involved Akt/ERK and Bcl-2/Bax pathways against oxidative damages in C6 glial cells

Abstract

Insulin, a hypoglycemic hormone, has multiple functions in the brain. The aim of this study to identify the mechanisms of insulin in hydrogen peroxide (H₂O₂)-induced toxicity in the C6 glial cells. Cytotoxicity, lactate dehydrogenase, nitric oxide, reactive oxygen species and calcium ion, lipid peroxidation, protein oxidation and glutathione levels were determined. Signaling pathway molecules were assessed by western blotting and RT-PCR. The results showed that treatment with insulin reduced the cell death and cell membrane damages against H₂O₂-induced toxicity. Furthermore, insulin interfered H₂O₂-induced intracellular generation of reactive oxygen species and calcium-ion transport, apoptosis, including lipid and protein oxidation products. Cells treated with insulin reverted H₂O₂-induced suppression of reduced glutathione levels by blocking oxidized glutathione. Moreover, insulin treatment activates Akt, restores ERK1/2 and Bcl-2 by preventing Bax and Bax/Bcl-2 ratio. Our results suggest that treatment of insulin exerts potential role against 24 h of H₂O₂-induced toxicity in C6 cells.

• Apoptosis
• glial cells
• insulin
• neuroprotection
• reactive oxygen species

Declaration of interest

The authors have no conflicts of interest to declare. This study was supported by Kyung Hee University (KHU-20131115) and Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2013R1A1A2006613).

Supplementary material available online

Supplementary Figure 1 and 2.