The Effect of Carbamazepine Against Glutamate-induced Cytotoxicity in the C6 Cell Line

Abstract

Purpose: Recent studies have shown that carbamazepine has positive effects on nervous system. However, its effect on glutamate-induced cytotoxicity in glial cells is still unclear. Our study was designed to investigate the effect of carbamazepine against glutamate-induced cytotoxicity in C6 glial cells and involved mechanisms. Material and Methods: In this study, the C6 glioma cell line was used. Four cell groups were prepared to evaluate the effect of carbamazepine on glial cell death after glutamate-induced cytotoxicity. The control group was without any treatment. Cells in the glutamate group were treated with 10 mM glutamate for 24 hours. Cells in the carbamazepine group were treated with various concentrations (3.75, 7.5, 15, and 30 μM) of carbamazepine for 24 hours. Cells in the carbamazepine + glutamate group were pre-treated with various concentrations (3.75, 7.5, 15, and 30 μM) of carbamazepine for 1 hour and then exposed to 10 mM glutamte for 24 hours. The cell viability was evaluated by XTT assay. Total antioxidant status (TAS), total oxidant status (TOS), tumor necrosis factor alpha (TNF-α), and malondialdehyde (MDA) levels in the cells were measured by commercial kits. Results: Carbamazepine at the concentration of 30 μM significantly increased the cell viability in C6 cells after glutamate-induce cytotoxicity (p < 0.05). CBZ (30 μM) + glutamate significantly increased TOS levels in C6 cells compared to control untreated control cells (p < 0.05), while it did not change TAS level (p > 0.05). Moreover, carbamazepine did not change TNF-α level (p > 0.05) and increased MDA (p< 0.05) level in C6 cells after glutamate-induced cytotoxicity. Conclusion: Carbamazepine decreases glial cell death after glutamate-induced cytotoxicity in C6 cells. While carbamazepine produced protective effective in the acute process, long-term usage may increase oxidative damage and cause cell death.

Special Issue of Health Sciences

DOI: 10.7176/JSTR/7-08-09