ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2014
β-Arrestin 2 mediates the anti-inflammatory effects of fluoxetine in lipopolysaccharide-stimulated microglial cells.
Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 33 citations in OpenAlex.
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- Modulation of microglial activation by antidepressants.Journal of psychopharmacology (Oxford, England) · 2022Review
- Longxuetongluo capsule alleviates lipopolysaccharide-induced neuroinflammation by regulating multiple signaling pathways in BV2 microglia cells.Journal of the Chinese Medical Association : JCMA · 2020Article
- The effect of fluoxetine on astrocyte autophagy flux and injured mitochondria clearance in a mouse model of depression.Cell death & disease · 2019Article
- Anti-neuroinflammatory effects of cudraflavanone A isolated from the chloroform fraction of Cudrania tricuspidata root bark.Pharmaceutical biology · 2018Article
- β-Arrestin Based Receptor Signaling Paradigms: Potential Therapeutic Targets for Complex Age-Related Disorders.Frontiers in pharmacology · 2018Review
- Hesperidin Alleviates Lipopolysaccharide-Induced Neuroinflammation in Mice by Promoting the miRNA-132 Pathway.Inflammation · 2016Article
- Fluoxetine Inhibits NLRP3 Inflammasome Activation: Implication in Depression.The international journal of neuropsychopharmacology · 2016Article
- Repurposing psychiatric medicines to target activated microglia in anxious mild cognitive impairment and early Parkinson's disease.American journal of neurodegenerative disease · 2016Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidence has suggested that microglial activation plays an important role in the pathogenesis of depression. Activated microglia can secrete various pro-inflammatory cytokines, which may contribute to the development and maintenance of depression. Thus, inhibition of microglial activation may have a therapeutic benefit in the treatment of depression. In the present study, we found that fluoxetine significantly inhibited lipopolysaccharide (LPS)-induced production of tumor necrosis factor-alpha (TNF-α), interleukin- 6 (IL-6) and nitric oxide (NO) and reduced the phosphorylation of transforming growth factor-beta-activated kinase 1 (TAK1) and nuclear factor-kappa B (NF-κB) p65 nuclear translocation in microglia. We further found that fluoxetine increased the expression of β-arrestin 2 and enhanced the association of β-arrestin 2 with TAK1-binding protein 1 (TAB1) and disrupted TAK1-TAB1 interaction. Moreover, β-arrestin 2 knock-down abolished the anti-inflammatory effects of fluoxetine in lipopolysaccharide-stimulated microglial cells. Collectively, our findings suggest that β-arrestin 2 is necessary for the anti-inflammatory effects of fluoxetine and offers novel drug targets in the convergent fluoxetine/β-arrestin 2 and inflammatory pathways for treating microglial inflammatory neuropathologies like depression.
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