Akademik Veri Yönetim Sistemi
5. ISPEC International Conference on Contemporary Scientific Research, Kayseri, Türkiye, 21 - 22 Nisan 2024, ss.97
ABSTRACT
Aim: Neurodegeneration is the progressive loss and structural deterioration of neuronal cells. Oxidative stress plays a role in the emergence of neurodegenerative diseases due to damage to neurons. Hydrogen peroxide (H2O2) superoxide radical it is formed by dismutation and causes oxidative stress. Venlafaxine, a serotonin and noradrenaline reuptake inhibitor, it is a drug that increases both serotonin and noradrenaline in the synaptic gap. The present study aimed to investigate the effect of venlafaxine on H2O2-induced cytotoxicity in C6 glioma cells. Materials and Methods: For the study, four groups were formed from glioma cells as control, venlafaxine at different concentrations (25, 50 and 100 µM), H2O2 (0,5 mM), and Venlafaxine+H2O2. In the study, TNF-α, IL-1β, NO and iNOS levels in the C6 glioma cells were determined. Results: H2O2-treated caused cytotoxicity in C6 glioma cell line; 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 TNF-α and IL-1β, which are inflammatory cytokines, it is observed that there is an increase in the H2O2 applied group and a significant decrease in the 100 μM Venlafaxine applied group. It is seen that NO and iNOS levels increased in the H2O2 applied group compared to the other groups. On the other hand, no statistical significance was found in the control, Venlafaxine and Venlafaxine+H2O2 groups.Conclusion: As a result, it was determined that venlafaxine treatment showed a protective effect in the H2O2-induced neural cytotoxicity model in C6 glioma cells.
Keywords: Cytotoxicity; C6 glioma cell; Venlafaxine; Hydrogen Peroxide