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Related Experiment Video

Updated: Aug 26, 2025

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Neuronal-microglial liver X receptor β activating decrease neuroinflammation and chronic stress-induced

Chunhui Li1, Huanghui Wu2, Ha Sen Ta Na3

  • 1Department of Anesthesiology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361102, PR China; Department of Anesthesiology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou 215000, PR China.

Brain Research
|October 10, 2022
PubMed
Summary
This summary is machine-generated.

Activating Liver X receptor beta (LXRβ) in neurons and microglia alleviates depression by reducing neuroinflammation. This involves inhibiting the NF-κB signaling pathway and NLRP3 inflammasome activation, crucial for treating stress-induced depression.

Keywords:
Basolateral amygdalaChronic unpredictable mild stressDepression-related behaviorLiver X receptor βMicrogliaNeuroinflammation

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Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Depression is linked to excessive neuroinflammation.
  • Liver X receptor beta (LXRβ) shows potential in modulating inflammation.
  • The precise mechanisms of LXRβ in alleviating neuroinflammation in depression are not fully understood.

Purpose of the Study:

  • To investigate the role of LXRβ in modulating neuroinflammation and depression-related behaviors.
  • To elucidate the underlying molecular mechanisms involving microglial activation and inflammatory pathways.
  • To assess the therapeutic potential of LXRβ activation in depression.

Main Methods:

  • Depression models in mice using chronic unpredictable mild stress (CUMS) and corticosterone (CORT).
  • Pharmacological activation of LXRβ using TO901317 and manipulation of microglia/neurons in the basolateral amygdala (BLA).
  • Assessment of behavioral tests, microglial activation, NF-κB signaling, NLRP3 inflammasome, and IL-1β release in vivo and in vitro.

Main Results:

  • CUMS and CORT induced depression-like behaviors with increased microglial activation, NF-κB and NLRP3 inflammasome activation, and IL-1β release in the BLA.
  • LXRβ activation significantly inhibited these inflammatory markers and behaviors.
  • Eliminating microglia or activating neurons in the BLA protected against depression-like behaviors.

Conclusions:

  • Pharmacological activation of neuronal-microglial LXRβ effectively alleviates depression-related behaviors.
  • This therapeutic effect is mediated by the modulation of neuroinflammation through the inhibition of NF-κB signaling and NLRP3 inflammasome activation.
  • LXRβ represents a promising therapeutic target for depression treatment by addressing neuroinflammation.