Akademik Veri Yönetim Sistemi
Molecular Biology Reports, cilt.53, sa.1, 2026 (SCI-Expanded, Scopus)
Background: Desvenlafaxine, a serotonin–norepinephrine reuptake inhibitor (SNRI) used for major depressive disorder, is the primary active metabolite of venlafaxine. While the immunomodulatory effects of the parent compound, venlafaxine, are well-documented, the direct impact of desvenlafaxine on macrophage-mediated inflammation remains less understood. This study aims to investigate whether desvenlafaxine influences pro-inflammatory cytokine production in activated macrophages. Methods: J774.2 macrophages were stimulated with lipopolysaccharide (LPS) to induce an inflammatory response and treated with desvenlafaxine at concentrations of 1, 5, and 10 µg/mL. Cell viability was assessed to ensure non-toxic dosing, and the concentrations of pro-inflammatory cytokines, including TNF-α, IL-6, IL-12p40, and GM-CSF, were quantified using Enzyme-Linked Immunosorbent Assay (ELISA). Results: Our results indicate that desvenlafaxine significantly inhibits the secretion of TNF-α and IL-6 in a concentration-dependent manner without affecting cell viability. Notably, IL-12p40 levels showed a significant reduction primarily at the lowest concentration (1 µg/mL). These findings suggest a selective anti-inflammatory effect on key macrophage-derived mediators under the tested conditions. Conclusions: Our findings suggest that desvenlafaxine possesses potential immunomodulatory properties by modulating pro-inflammatory cytokine release. This study provides preliminary evidence that its therapeutic benefits in depression may involve neuroinflammatory pathways beyond classical neurotransmission, although further research is required to clarify the underlying mechanisms.