Fig. 9

Diagram of the proposed molecular mechanism of the anti-depressive effect of KJG. In physiological status, TLR4 and PI3K/AKT signaling pathways are inactivated, and the increased secretion of pro-inflammatory factors (TNF-α, IL-6, IL-1β) is not observed. After CUMS and LPS exposure, the TLR4 pathway is triggered, followed by the PTEN-induced inhibition of the PI3K/AKT signaling pathway and the promoted transcriptional activity of FOXO1, as well as the increased secretion of pro-inflammatory factors. Conversely, the KJG-mediated anti-depressant effect can decrease TLR4 but increase PI3K/AKT expression levels, inhibiting FOXO1 activity by promoting nuclear exportation and reducing pro-inflammatory secretion factors