The proposed pathway is shown in Fig. 11, and we demonstrated that baicalin could improve depressive-like behavior and ameliorate neuroinflammation in a CUMS and LPS-induced mice model of depression via the inhibition of pernicious overexpression of TLR4 via the PI3K/AKT/FoxO1 pathway. The gene discussed is AKT1; the disease is depressive symptom measurement.