Brain research · 2026
Antidepressant mechanism of secoisolariciresinol in corticosterone-induced mice: PTGS2 as a key target of the cAMP-PKA-CREB-BDNF pathway.
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Tuo Yan-Jun, Meng Zi, A Ru-Han, Zhai Shu-Ting, Wang Mu-Lan, Zha Chen-Liang, Zou En-Guo, He Bei-Lan, Feng Ye-Meng, Zeng Xiao-Long, Li Jun, Gong Qin
Аннотация
OBJECTIVE: Secoisolariciresinol (SECO), a natural monomer from Syringa oblata Lindl, remains unclear in antidepressant effects. This study aimed to investigate the antidepressant mechanism of SECO and clarify its core target and signaling pathway.
METHODS: Network pharmacology, molecular docking and corticosterone (CORT)-induced depressive mice model were applied. Behavioral tests, histological staining, ELISA and Western blot were performed for evaluation.
RESULTS: Behavioral tests confirmed that SECO significantly improved depressive-like behaviors, increased sucrose preference and exploratory ability, and reduced immobility time. SECO ameliorated hippocampal CA1 neuronal morphological damage and neuronal loss. Treatment with SECO significantly decreased serum corticosterone (CORT) concentrations and hippocampal prostaglandin E2 (PGE2) levels. Concurrently, it elevated serum levels of key neurotransmitters, namely serotonin (5-HT), norepinephrine (NE), and dopamine (DA), and increased cyclic adenosine monophosphate (cAMP) content in the hippocampus. Mechanistically, SECO downregulated the expression of prostaglandin-endoperoxide synthase 2 (PTGS2) and activated the cAMP-PKA-CREB-BDNF signaling cascade.
CONCLUSION: SECO alleviates neuroinflammation via PTGS2 inhibition and enhances neuronal plasticity by activating the cAMP/PKA-CREB-BDNF signaling pathway. These two synergistic effects contribute to the neuroprotective action of SECO, thereby ameliorating CORT-induced depressive-like behaviors in mice.
METHODS: Network pharmacology, molecular docking and corticosterone (CORT)-induced depressive mice model were applied. Behavioral tests, histological staining, ELISA and Western blot were performed for evaluation.
RESULTS: Behavioral tests confirmed that SECO significantly improved depressive-like behaviors, increased sucrose preference and exploratory ability, and reduced immobility time. SECO ameliorated hippocampal CA1 neuronal morphological damage and neuronal loss. Treatment with SECO significantly decreased serum corticosterone (CORT) concentrations and hippocampal prostaglandin E2 (PGE2) levels. Concurrently, it elevated serum levels of key neurotransmitters, namely serotonin (5-HT), norepinephrine (NE), and dopamine (DA), and increased cyclic adenosine monophosphate (cAMP) content in the hippocampus. Mechanistically, SECO downregulated the expression of prostaglandin-endoperoxide synthase 2 (PTGS2) and activated the cAMP-PKA-CREB-BDNF signaling cascade.
CONCLUSION: SECO alleviates neuroinflammation via PTGS2 inhibition and enhances neuronal plasticity by activating the cAMP/PKA-CREB-BDNF signaling pathway. These two synergistic effects contribute to the neuroprotective action of SECO, thereby ameliorating CORT-induced depressive-like behaviors in mice.