Background <p>The relationship between psychiatric disorders and the immune system has become increasingly recognized, with inflammatory pathways implicated in disease pathogenesis, therapeutic response, and progression. Amisulpride, an atypical antipsychotic preferentially acting as an antagonist on postsynaptic D2/D3 receptors, has been widely studied for its psychiatric effects, whereas its immunomodulatory properties remain largely unexplored.</p> Aim <p>We investigated the potential immunomodulatory effects of amisulpride on J774.2 macrophage cells.</p> Methods <p>J774.2 macrophage cells were treated with amisulpride at concentrations of 1, 5, and 10 μg/mL for 24 hours. Cytotoxicity was assessed, and proinflammatory cytokine production (TNF-α, GMCSF, IL-6, IL-12p40) was measured by ELISA under both basal and LPS-induced inflammatory conditions. </p> Results <p>Amisulpride demonstrated no cytotoxicity at any concentration. Under non-inflammatory conditions, cytokine levels remained unchanged. In contrast, upon LPS-induced inflammation, amisulpride elicited a dose-dependent anti-inflammatory response, significantly reducing cytokine secretion. Conclusion: Amisulpride exhibits immunomodulatory activity under inflammatory conditions. These findings suggest a potential anti-inflammatory mechanism that warrants further investigation.</p>

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Immunomodulatory effects of amisulpride on mammalian macrophages

  • Mehmet Buğrahan Gürcan,
  • Nur Ekimci Gürcan,
  • Fatma Sude Özarslan,
  • Berk Gökçe,
  • Beyza Nur Özpamukçu,
  • Esra Aydemir,
  • Furkan Ayaz

摘要

Background

The relationship between psychiatric disorders and the immune system has become increasingly recognized, with inflammatory pathways implicated in disease pathogenesis, therapeutic response, and progression. Amisulpride, an atypical antipsychotic preferentially acting as an antagonist on postsynaptic D2/D3 receptors, has been widely studied for its psychiatric effects, whereas its immunomodulatory properties remain largely unexplored.

Aim

We investigated the potential immunomodulatory effects of amisulpride on J774.2 macrophage cells.

Methods

J774.2 macrophage cells were treated with amisulpride at concentrations of 1, 5, and 10 μg/mL for 24 hours. Cytotoxicity was assessed, and proinflammatory cytokine production (TNF-α, GMCSF, IL-6, IL-12p40) was measured by ELISA under both basal and LPS-induced inflammatory conditions.

Results

Amisulpride demonstrated no cytotoxicity at any concentration. Under non-inflammatory conditions, cytokine levels remained unchanged. In contrast, upon LPS-induced inflammation, amisulpride elicited a dose-dependent anti-inflammatory response, significantly reducing cytokine secretion. Conclusion: Amisulpride exhibits immunomodulatory activity under inflammatory conditions. These findings suggest a potential anti-inflammatory mechanism that warrants further investigation.