Our study showed that SY prevents depression-like symptoms in CUMS-exposed rats by preventing HPA dysfunction, decreasing the neurotransmitter levels, minimizing oxidative stress, suppressing neuroinflammation, and activating the PI3K/Akt/mTOR-mediated BDNF/TrkB pathway, all of which are the key players in the pathological basis of depression. The gene discussed is NTRK2; the disease is depressive disorder.