Effect of Qingyangshen glycosides on social defeat mice model

原肌球蛋白受体激酶B 社会失败 FNDC5 脑源性神经营养因子 神经营养因子 下调和上调 开阔地 蛋白激酶A 氧化应激 受体 内分泌学 内科学 化学 生物 医学 细胞生物学 激酶 生物化学 纤维连接蛋白 基因 细胞外基质
作者
Dingding Liu,Jingru Wang,Lulu Chang,Qiang Zhu,Ning Jiang,Mudassar Azhar,Guirong Zeng
出处
期刊:Journal of Ethnopharmacology [Elsevier]
卷期号:293: 115253-115253 被引量:4
标识
DOI:10.1016/j.jep.2022.115253
摘要

Qingyangshen (Cynanchum otophyllum C.K.Schneid.PI.Wilson.) is the folk medicine of Yunnan which is renowned for its use in the management of neuropsychiatric diseases. The isolated glycosides from Qingyangshen have demonstrated relief in the social defeat stress, however, mechanism of action has not yet been elucidated.This study is aimed to elucidate the effect of Qingyangshen glycosides (QYS) on chronic social defeat stress (CSDS)-induced depression-like symptoms and the related mechanism.In mice, CSDS model was developed, and the effect of QYS was evaluated by observing the behavioral performance of these mice exposed to tasks related to depression-like activities. Moreover, microscopic pathological examinutesation was also done. Furthermore, the protein expressions related to social defeat stress were also determined to elucidate the possible underlying mechanism.Our results indicated that QYS treatment reversed the CSDS-induced depressive-like behaviors as measured by the increased sucrose preference, open field activity, and social interactions among mice. The reversal of the morphological changes in the hippocampus of the CSDS mice was also noted. Additionally, QYS treatment also upregulated the silent mating type information regulation 2 homolog 1 (SIRT1), peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), fibronectin III domain containing protein 5 (FNDC5), brain-derived neurotrophic factor (BDNF), tropomyosin-related kinase B (TrkB), and mitogen-activated protein kinase (MAPK) proteins.Our study indicated that QYS had a good anti-social defeat stress effect on CSDS-induced depression in mice, mainly through SIRT1/PGC-1α/FNDC5/BDNF-TrkB signaling pathway activation.
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