# Therapeutic potential of trazodone in trigeminal neuralgia based on inflammation and oxidative stress: an in vitro experimental study

## TL;DR

This study explores how trazodone, a drug with neuroprotective properties, may help treat trigeminal neuralgia by reducing inflammation and oxidative stress in glial cells.

## Contribution

The study reveals trazodone's anti-inflammatory and antioxidant effects in trigeminal neuralgia via the MAPK pathway in BV-2 glial cells.

## Key findings

- Trazodone inhibited BV-2 cell growth and reduced inflammation markers TNF-α, IL-6, and IL-1β.
- Trazodone decreased oxidative stress by lowering ROS levels in LPS-treated BV-2 cells.
- Trazodone suppressed the MAPK pathway, which is linked to inflammation and cell proliferation.

## 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.