Characterization of Inflammatory Signals in BV-2 Microglia in Response to Wnt3a

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.Keywords:neuroinflammation;microglial activation;Wnt3a;β-catenin

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