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Figure 8 | Journal of Neuroinflammation

Figure 8

From: Lithium ameliorates lipopolysaccharide-induced microglial activation via inhibition of toll-like receptor 4 expression by activating the PI3K/Akt/FoxO1 pathway

Figure 8

Schematic illustration of lithium-mediated suppression of neuroinflammation. FoxO1 maintains lipopolysaccharide (LPS)-triggered TLR4-mediated inflammation signaling. LPS inactivates microglial FoxO1 by inducing PI3K/Akt signaling, which triggers the phosphorylation and nuclear exclusion of FoxO1. The TLR4-PI3K/Akt-FoxO1 axis provides a self-limiting mechanism by which macrophages avoid inappropriate overactivation of inflammation after initiation of the inflammatory response. Lithium, an activator of PI3K/Akt signaling, enhances the self-limiting mechanism and inhibits the activation of microglia. TLR4, toll-like receptor 4; ➞, lead to/activate; ⊣, inhibit.

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