Neuropsychiatric disease and treatment · 2026
Echinocystic Acid Antagonizes Post-Stroke Depression in Mice by Suppressing the JNK/NF-κB Signaling Pathway.
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Wang Dandan, Li Wei, Zhang Xuan, Zhu Kaiqi, Wang Yuzhen, Cai Yaozhuo, Chen Hao, Cai Xueli, Sun Jingping
Аннотация
BACKGROUND: Post-stroke depression (PSD), a common neuropsychiatric complication after stroke, affects approximately one-third of stroke survivors and severely impairs recovery and quality of life. Echinocystic acid (EA), a pentacyclic triterpenoid from various medicinal herbs, exhibits anti-inflammatory and anti-depressant properties. However, whether EA exerts neuroprotective and antidepressant effects in PSD remains unknown.
OBJECTIVE: This study aims to determine whether EA alleviates PSD and to explore its potential mechanisms involving the JNK/NF-κB pathway and inflammatory cytokines.
METHODS: PSD was modeled using middle cerebral artery occlusion/reperfusion (MCAO/R) combined with chronic unpredictable mild stress (CUMS). Following MCAO/R surgery, animals received daily intraperitoneal injections of EA or EA combined with the JNK agonist anisomycin (AN) for 28 consecutive days. The expression of phosphorylated JNK (p-JNK) and phosphorylated NF-κB (p-NF-κB) was analyzed by Western blotting. The levels of inflammatory cytokines, including IL-1β, IL-6, and TNF-α, were measured using enzyme-linked immunosorbent assay (ELISA). Depressive-like behaviors and the therapeutic efficacy of EA were assessed through a series of behavioral tests. Furthermore, neuronal necrosis and Nissl body integrity were observed using hematoxylin-eosin (H&E) and Nissl staining, respectively.
RESULTS: EA treatment significantly downregulated the expression of p-JNK, p-NF-κB, and inflammatory cytokines. H&E staining revealed that EA reduced neuronal necrosis in the hippocampal dentate gyrus. Consistently, Nissl staining demonstrated that EA increased the number of Nissl bodies in the same region. Furthermore, EA administration alleviated depressive-like behaviors in PSD mice. However, the administration of AN counteracted the suppressive effects of EA on the JNK/NF-κB signaling pathway and reversed the beneficial behavioral outcomes associated with EA treatment.
CONCLUSION: The results indicate that EA mitigates neuronal necrosis, alleviates depression-like behaviors, and alleviates PSD by suppressing JNK/NF-κB pathway activation and inflammatory cytokine production.
OBJECTIVE: This study aims to determine whether EA alleviates PSD and to explore its potential mechanisms involving the JNK/NF-κB pathway and inflammatory cytokines.
METHODS: PSD was modeled using middle cerebral artery occlusion/reperfusion (MCAO/R) combined with chronic unpredictable mild stress (CUMS). Following MCAO/R surgery, animals received daily intraperitoneal injections of EA or EA combined with the JNK agonist anisomycin (AN) for 28 consecutive days. The expression of phosphorylated JNK (p-JNK) and phosphorylated NF-κB (p-NF-κB) was analyzed by Western blotting. The levels of inflammatory cytokines, including IL-1β, IL-6, and TNF-α, were measured using enzyme-linked immunosorbent assay (ELISA). Depressive-like behaviors and the therapeutic efficacy of EA were assessed through a series of behavioral tests. Furthermore, neuronal necrosis and Nissl body integrity were observed using hematoxylin-eosin (H&E) and Nissl staining, respectively.
RESULTS: EA treatment significantly downregulated the expression of p-JNK, p-NF-κB, and inflammatory cytokines. H&E staining revealed that EA reduced neuronal necrosis in the hippocampal dentate gyrus. Consistently, Nissl staining demonstrated that EA increased the number of Nissl bodies in the same region. Furthermore, EA administration alleviated depressive-like behaviors in PSD mice. However, the administration of AN counteracted the suppressive effects of EA on the JNK/NF-κB signaling pathway and reversed the beneficial behavioral outcomes associated with EA treatment.
CONCLUSION: The results indicate that EA mitigates neuronal necrosis, alleviates depression-like behaviors, and alleviates PSD by suppressing JNK/NF-κB pathway activation and inflammatory cytokine production.