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Figure 9

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Publication: Molagoda et al., 2021 - Fisetin inhibits lipopolysaccharide-induced inflammatory response by activating β-catenin, leading to a decrease in endotoxic shock
All Figures: Figures for Molagoda et al., 2021

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Figure 9

Fisetin inhibits GSK-3β-mediated NF-κB activation in the presence of β-catenin, leading to the inhibition of inflammation-induced septic shock. Once macrophages are exposed to high concentrations of the bacterial endotoxin, LPS, they initiate an inflammatory response and endotoxic shock by upregulating the expression of NF-κB-induced inflammatory genes, such as iNOS, COX-2, IL-12, IL-6, and TNF-α. Fisetin binds to the noncompetitive ATP-binding sites of GSK-3β and phosphorylates GSK-3β at Ser9, resulting in the inactivation GSK-3β and release of β-catenin from the destruction complex. The released β-catenin inhibits the transcriptional activity of NF-κB, thereby alleviating LPS-induced inflammation and endotoxic shock.

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