ArticleBiomedicines2023
Characterization of Inflammatory Signals in BV-2 Microglia in Response to Wnt3a.
Article in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Comparative Analysis of LPS/IFN-γ and LPS/ATP-Induced Inflammatory Models in BV2 Microglia.Neurochemical research · 2026Article
- A novel peptide-compound conjugate alleviates endotoxin-induced inflammation via NF-κB/MAPK modulation.Journal of molecular medicine (Berlin, Germany) · 2025Article
- SMART-Guided Isolation and Identification of Seven-Membered Cembranolides with Anti-Inflammation Activity from the Soft CoralMarine drugs · 2025Article
- In Vitro Assessment of Cholinesterase Inhibition and Neuroprotective Effects of Elaeocarpus angustifolius Blume Against Amyloid-Beta Peptide-Induced Toxicity in SH-SY5Y and BV-2 Cells.Neurochemical research · 2025Article
- Comparative activity of dimethyl fumarate derivative IDMF in three models relevant to multiple sclerosis and psoriasis.FEBS open bio · 2025Article
- Psilocin, the Psychoactive Metabolite of Psilocybin, Modulates Select Neuroimmune Functions of Microglial Cells in a 5-HTMolecules (Basel, Switzerland) · 2024Article
- Tet1-mediated 5hmC regulates hippocampal neuroinflammation via wnt signaling as a novel mechanism in obstructive sleep apnoea leads to cognitive deficit.Journal of neuroinflammation · 2024Article
- Blood-activating, depression-relieving formula alleviates post-stroke depression: mechanistic insights from network pharmacology and microglial validation.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Activation of microglia is one of the pathological bases of neuroinflammation, which involves various diseases of the central nervous system. Inhibiting the inflammatory activation of microglia is a therapeutic approach to neuroinflammation. In this study, we report that activation of the Wnt/β-catenin signaling pathway in a model of neuroinflammation in Lipopolysaccharide (LPS)/IFN-γ-stimulated BV-2 cells can result in inhibition of production of nitric oxide (NO), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). Activation of the Wnt/β-catenin signaling pathway also results in inhibition of the phosphorylation of nuclear factor-κB (NF-κB) and extracellular signal-regulated kinase (ERK) in the LPS/IFN-γ-stimulated BV-2 cells. These findings indicate that activation of the Wnt/β-catenin signaling pathway can inhibit neuroinflammation through downregulating the pro-inflammatory cytokines including iNOS, TNF-α, and IL-6, and suppress NF-κB/ERK-related signaling pathways. In conclusion, this study indicates that the Wnt/β-catenin signaling activation may play an important role in neuroprotection in certain neuroinflammatory diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.