ArticleMolecular biology reports2023
Inhibitory effects of fluoxetine on the secretion of inflammatory mediators and JAK/STAT3 and JNK/TLR4 gene expression.
Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Repurposing Selective Serotonin Reuptake Inhibitors as Immunomodulators: Effects on Macrophage Activation and Polarization.Molecular neurobiology · 2026Review
- Exploration and Validation of the Diagnostic Potential of the Circadian Rhythm-Related Genes CCL23 and VNN1 in Adolescents with Depressive Disorder.Molecular neurobiology · 2026Article
- Neuro-Immune Crosstalk: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Article
- Serum inflammatory cytokines in the progression of depression.Frontiers in immunology · 2026Review
- Inflammatory models of depression in rodents and humans.Frontiers in psychiatry · 2026Review
- Neuroprotective Effects of Fluoxetine Derivative 4-[3-Oxo-3-(2-trifluoromethyl-phenyl)-propyl]-morpholinium Chloride (OTPM) as a Potent Modulator of Motor Deficits and Neuroinflammatory Pathways in LPS-Induced BV-2 Microglial Cells and MPTP-Induced Parkinsonian Models.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Screening of the FDA-approved drug library identifies CCL17 inhibitors that block arthritic pain.Scientific reports · 2025Article
- Interconnections of screen time with neuroinflammation.Molecular and cellular biochemistry · 2025Review
- Fluoxetine promotes IL-10-dependent metabolic defenses to protect from sepsis-induced lethality.Science advances · 2025Article
- Article
- Steroids for the Treatment of Misophonia and Misokinesia.Case reports in psychiatry · 2024Article
- Fluoxetine promotes immunometabolic defenses to mediate host-pathogen cooperation during sepsis.bioRxiv : the preprint server for biology · 2023Article
- JAK-STAT signaling in inflammation and stress-related diseases: implications for therapeutic interventions.Molecular biomedicine · 2023Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSelective serotonin reuptake inhibitors (SSRIs) are the most common class of medicines used for the treatment of major depression. Recent studies have reported an association between depression and inflammation and suggested the significant effects of SSRIs on inflammatory processes.
methodsThe current study aimed to evaluate the effects of fluoxetine, an SSRI, on the level of inflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), in the rat serum and RAW264.7 mouse macrophage cell line, using ELISA sandwich assays. Also, the expression of inflammatory genes, including JAK/STAT3 and TLR4/JNK, was examined in macrophages, using real-time quantitative reverse transcription PCR to determine the potential mechanism of fluoxetine in inflammation. The rats received fluoxetine (10, 20, and 40 mg/kg) 30 min before lipopolysaccharide (LPS) treatment for 90 min. The cells received different doses of fluoxetine (5, 10, and 20 µg/mL) before stimulation with LPS for 24 or 48 h.
resultsThe serum concentrations of IL-1β, IL-6, and TNF-α were reduced in rats and cells treated with fluoxetine. Following fluoxetine administration, the expression of JAK/STAT3 and TLR4/JNK genes was significantly decreased in the RAW264.7 cells treated with LPS for 24 h. However, after 48 h of treatment with LPS, fluoxetine failed to diminish the elevated expression of JAK and JNK genes, while it significantly decreased the expression of STAT3 and TLR4 genes.
conclusionThe findings revealed that fluoxetine has anti-inflammatory properties, mainly due to the reduction of inflammatory cytokines and inhibition of JAK/STAT3 and TLR4/JNK gene expression in macrophages.
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