Brain Sciences (Oct 2022)

Suppressive Effects of Isofraxidin on Depressive-like Behaviors Induced by Chronic Unpredictable Mild Stress in Mice

  • Xiaoli Wu,
  • Jingwen Gu,
  • Zhicong Zou,
  • Meng Yu,
  • Chen Zhang,
  • Qinghui Xiao,
  • Xin Chen,
  • Chuwen Li

DOI
https://doi.org/10.3390/brainsci12101376
Journal volume & issue
Vol. 12, no. 10
p. 1376

Abstract

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Isofraxidin is an active component of several traditional and functional plants that have beneficial properties for neurodegenerative diseases. In this study, we examined whether isofraxidin exhibited antidepressant-like effects in chronic unpredictable mild stress (CUMS)-induced mice. Firstly, isofraxidin could reverse CUMS-induced decrease in body weight gain in mice. Additionally, in the sucrose preference test (SPT), isofraxidin reversed the decrease in sucrose consumption due to CUMS-induced depressive-like behavior. Isofraxidin also increased locomotor activity in the open field test (OFT) and alleviated immobility duration in the forced swimming test (FST) and tail-suspension test (TST). Furthermore, isofraxidin decreased levels of corticosterone (CORT), adrenocorticotropic hormone (ACTH), and hypothalamus corticotrophin-releasing hormone (CRH) in the serum after CUMS-induced hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis. Also, isofraxidin suppresses tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 expression in the hippocampus of CUMS mice. Further investigations demonstrated that isofraxidin inhibited CUMS-induced activation of nuclear factor kappa B (NF-κB) and NOD-like receptor protein 3 (NLRP3) inflammasomes in the hippocampus. Summarily, in CUMS-induced mice, isofraxidin reduced depressive-like behaviors, accompanied by its inhibitory effects on hyperactivity of the HPA axis and NF-κB /NLRP3 inflammasomes pathways.

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