Amentoflavone Exerts Anti-Neuroinflammatory Effects by Inhibiting TLR4/MyD88/NF-<i>κ</i>B and Activating Nrf2/HO-1 Pathway in Lipopolysaccharide-Induced BV2 Microglia

<div>Effects of amentoflavone on the expression of Nrf2/HO-1 levels in LPS-treated BV2 microglial cells. (a–c) Semiquantitative analysis of the relative levels of MDA, GSH, and SOD. (d) Representative immunoblots of Keap1, Nrf2, and HO-1 proteins in BV2 microglial cells. (e) BV2 microglial cells were treated with amentoflavone (10 <i>μΜ</i>) or 0.5% DMSO for 1 h, followed by treatment with LPS (1 <i>μ</i>g/ml) or PBS for 6 h. Semiquantitative analysis of the relative levels of Keap1, Nrf2, and HO-1 by densitometric analysis. 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All experiments were performed in triplicate. LPS: lipopolysaccharide; AF: amentoflavone.</div>

Mediators of Inflammation

fig5

Figure 5

Figure 5: Amentoflavone Exerts Anti-Neuroinflammatory Effects by Inhibiting TLR4/MyD88/NF-<i>κ</i>B and Activating Nrf2/HO-1 Pathway in Lipopolysaccharide-Induced BV2 Microglia 

Figure 5 | Amentoflavone Exerts Anti-Neuroinflammatory Effects by Inhibiting TLR4/MyD88/NF-κB and Activating Nrf2/HO-1 Pathway in Lipopolysaccharide-Induced BV2 Microglia 