This analysis demonstrates vortioxetine's effects on inflammation and TLR4/NF-κB signaling in enteric glial cells.
Parkinson’s disease (PD) is a progressive neurodegenerative disorder with both motor and non-motor symptoms, and currently, there is currently no disease-modifying therapy. Due to their potential anti-inflammatory effects, antidepressants have gained attention as therapeutic agents in inflammation-related neurological conditions. In this study, we aimed to investigate the effects of vortioxetine on rotenone-induced enteric inflammation in an in vitro model using enteric glial cells and whether these effects involve modulation of the TLR4/NF-κB signaling pathway. Cells were treated with rotenone (10 μM) and vortioxetine (1 and 5 μM). TLR4 and NF-κB mRNA expression levels were analyzed by RT-qPCR, and the levels of TNF-α, IL-1β, and IL-6 were measured via ELISA. The findings showed that rotenone significantly suppressed TLR4 and NF-κB expression by impairing the immune responses of glial cells, and the administration of 5 μM vortioxetine further enhanced this effect. Additionally, the decrease observed in TNF-α and IL-1β levels in the rotenone groups was reversed by vortioxetine administration. The results suggest that vortioxetine may regulate inflammatory responses in enteric glial cells through the TLR4/NF-κB pathways and could be investigated as a potential therapeutic compound in inflammation-based models of the gut-brain axis in PD.
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Samur et al. (2025) studied this question.
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