Abstract
Trigeminal neuralgia (TN) is a debilitating condition affecting the patients' life quality. New therapeutic approaches and novel drugs are required to treat TN. Trazodone being a serotonin antagonist and reuptake inhibitor (SARI) provides neuroprotection, however its role and underlying mechanism in TN in vitro or in vivo are not clear. This study was aimed to investigate the trazodone impact on glial BV-2 cells regarding TN. It was found that trazodone inhibited the BV-2 cells growth and suppressed the inflammation and oxidative stress in Lipopolysaccharide (LPS)-treated BV-2 cells. Trazodone treatment specifically decreased the levels of Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6 (IL-6), Interleukin-1 beta (IL-1β) (p < 0.05), and Reactive Oxygen Species (ROS) (p < 0.01). Moreover, trazodone suppressed the Mitogen-Activated Protein Kinase (MAPK) pathway in LPS-treated BV-2 cells. These outcomes demonstrate that trazodone suppressed glial cell hyperproliferation, inflammation, and oxidative stress through MAPK pathway activation.