Abstract

Aim: Neurodegeneration is the progressive loss and structural deterioration of neuronal cells. Hydrogen peroxide (H2O2) is formed by dismutation and causes oxidative stress in neuronal cells. Venlafaxine is a drug that increases both serotonin and noradrenaline in the synaptic gap.In this study, the effect of venlafaxine on H2O2-induced cytotoxicity in C6 cells was investigated. Methods: First of all, different doses of venlafaxine (25, 50, and 100 µM) were tried to find the appropriate dose in C6 glioma cells. Then, the effect of venlafaxine on H2O2-induced cytotoxicity in the cells was investigated. For this purpose, cell viability rate, proinflammatory markers IL-1β and TNF-α, and NO and iNOS levels were examined by ELISA kits. Results: H2O2-treated caused cytotoxicity in the C6 glioma cells; when venlafaxine 25, 50, and 100 μM doses were evaluated in terms of cell viability, it was observed that the 100 μM venlafaxine applied group significantly increased cell viability compared to the other groups. When we look at the levels of IL-1β and TNF-α, it is observed that there is an increase in the H2O2 applied group and a significant decrease in the venlafaxine (100 μM) applied group. It was observed that NO and iNOS levels increased in the H2O2 applied group compared to the other groups. It was observed that Venlafaxine treatment reduced the increased NO and iNOS levels caused by H2O2. Conclusion: The study results showed that venlafaxine may have a protective effect on H2O2-induced cytotoxicity in C6 glioma cells.

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