4.7 Article

The effect of geniposide on chronic unpredictable mild stress-induced depressive mice through BTK/TLR4/NF-κB and BDNF/TrkB signaling pathways

Journal

PHYTOTHERAPY RESEARCH
Volume 35, Issue 2, Pages 932-945

Publisher

WILEY
DOI: 10.1002/ptr.6846

Keywords

BDNF/TrkB pathway; BTK/TLR4/NF-kappa B pathway; CUMS; depression; Geniposide; PC12 cells

Funding

  1. Fundamental Research Funds for the Central Universities [2632017PY14]
  2. National Natural Science Foundation [81673434]
  3. Double First-Class University project [CPU2018GY22]

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The study demonstrated that geniposide could improve depressive symptoms in CUMS-induced mice by regulating inflammatory cytokines and oxidative stress. Additionally, geniposide affected various protein kinases and signaling pathways, exerting an antidepressant effect.
The purpose of this study was to estimate the pharmacological effect of geniposide (GEN) on depression, caused by chronic unpredictable mild stress (CUMS), and explore its potential mechanism. During the 6 week CUMS procedure, the mice were treated with GEN (10, 40 mg/kg) by gavage once daily for 3 weeks. As a result, the GEN treatment remarkably improved the behavioral manifestations and suppressed the generations of inflammatory cytokines both in vivo and in vitro. The MDA level was significantly increased, while the activities of SOD, GSH-PX were decreased in CUMS-challenged mice and corticosterone-stimulated PC12 cells. GEN administration significantly inhibited those changes. Moreover, GEN treatment could downregulate the expressions of p-BTK, TLR4, MyD88, p-NF-kappa B proteins, and upregulate BDNF, p-TrkB generations in CUMS-induced mice. Moreover, GEN administration inhibited the protein levels of p-BTK, TLR4, MyD88, p-NF-kappa B in corticosterone-induced PC12 cell. In summary, the results suggested that GEN exerted a therapeutic effect on CUMS-induced depressive mice possibly through the regulation of BTK/TLR4/NF-kappa B and BDNF/TrkB signaling pathways.

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