Silibinin exerts antidepressant effects by improving neurogenesis through BDNF/TrkB pathway - PubMed (original) (raw)

. 2018 Aug 1:348:184-191.

doi: 10.1016/j.bbr.2018.04.025. Epub 2018 Apr 20.

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Silibinin exerts antidepressant effects by improving neurogenesis through BDNF/TrkB pathway

Yan-Jiao Li et al. Behav Brain Res. 2018.

Abstract

Classic antidepressants benefit depression patients partially by improving neurogenesis and/or brain-derived neurotrophic factor (BDNF)/TrkB pathway which were impaired in depression. In this study, we demonstrated that Silibinin (SLB), a polyphenolic flavanoid from Silybum marianum, ameliorated reserpinized mouse depressant-like behaviors. The antidepressants of SLB administration was associated with increased neural stem cells (NSCs) proliferation and further confirmed in BDNF/TrkB signaling transduction. SLB treatment reversed the decreased expression levels of BDNF and its receptor TrkB, and the reduced activation of downstream target proteins including phosphorylated extracellular-regulated protein kinase (p-ERK) and phosphorylated cAMP-response element binding protein (p-CREB) in depressived hippocampus. Furthermore, intracerebroventricular injection of GNF5837, a TrkB antagonist, abrogated antidepressant-like effects of SLB in mice along with the improved NSC proliferation, as well as enhanced levels of p-ERK and p-CREB in mice hippocampus. Taken together, these results suggest that SLB may exert antidepressant effects through BDNF/TrkB signaling pathway to improve NSC proliferation in acute depression.

Keywords: Acute depression; Brain-derived neurotrophic factor; Neural stem cell; Neurogenesis; Silibinin; TrkB.

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