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
Home>Characterization of Inflammatory Signals in BV-2 Microglia in Response to Wnt3a
Characterization of Inflammatory Signals in BV-2 Microglia in Response to Wnt3a
- Impact factors: 7
- Publication: Journal of Animal Science and Biotechnology
- Author:Ma Xinhao, Yang Xinran, Zhang Dianqi, Zhang Wenzhen, Wang Xiaoyu, Xie Kuncheng, He Jie, Mei Chugang, Zan Linsen
- DOI citation-doi:10.1186/s40104-022-00820-1
- Date:2023-02-03T00:00:00.000Z