Furthermore, network pharmacology analysis suggested that the PI3K-AKT signaling pathway may contribute to the protective effects of FGE against METH-induced neuronal injury.<h4>Conclusion</h4>This study demonstrates that FGE, a potential natural agent, alleviates anxiety- and depression-like behaviors induced by METH through the reduction of neuroinflammation in the hippocampus. The gene discussed is AKT1; the disease is depressive symptom measurement.