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Ganoderic Acid A Attenuates LPS-Induced Neuroinflammation in BV2 Microglia by Activating Farnesoid X Receptor

Yue Jia1, Dandan Zhang1, Hua Yin2

  • 1School of Medicine, Yunnan University, 2 Cuihu North Road, Kunming, 650091, Yunnan, People's Republic of China.

Neurochemical Research
|April 6, 2021
PubMed

Insights

Ganoderic acid A (GAA) reduces neuroinflammation by activating the farnesoid-X-receptor (FXR) in microglia. This compound suppresses pro-inflammatory responses and promotes beneficial M2 microglial states, offering therapeutic potential for neurodegenerative diseases.

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Neuroinflammation, primarily driven by microglia, is a key factor in neurodegenerative diseases.
  • Ganoderic acid A (GAA), from Ganoderma lucidum, has shown anti-inflammatory effects in other conditions.
  • The role of GAA in neuroinflammation and its underlying mechanisms remain largely unexplored.

Purpose of the Study:

  • To investigate the anti-neuroinflammatory effects of GAA on lipopolysaccharide (LPS)-stimulated BV2 microglial cells.
  • To elucidate the molecular mechanisms by which GAA modulates microglial activation and inflammatory responses.
  • To explore the potential of GAA as a therapeutic agent for neuroinflammatory disorders.

Main Methods:

  • Utilized LPS-stimulated BV2 microglial cells as an in vitro model of neuroinflammation.
  • Assessed the effects of GAA on microglial proliferation, activation, and M1/M2 polarization.
  • Measured the release of pro-inflammatory cytokines and the expression of brain-derived neurotrophic factor (BDNF).
  • Investigated the role of the farnesoid-X-receptor (FXR) pathway using specific antagonists and siRNA.

Main Results:

  • GAA significantly suppressed LPS-induced BV2 microglial proliferation and activation.
  • GAA promoted the M1 to M2 microglial phenotype conversion.
  • GAA inhibited pro-inflammatory cytokine release and enhanced BDNF expression.
  • FXR expression was downregulated by LPS, and FXR antagonism reversed GAA's beneficial effects.

Conclusions:

  • Ganoderic acid A (GAA) exhibits significant anti-neuroinflammatory properties in microglia.
  • GAA exerts its effects by activating the farnesoid-X-receptor (FXR) pathway.
  • These findings highlight GAA's potential therapeutic value for neurodegenerative diseases characterized by neuroinflammation.
Keywords:
BV2 MicrogliaFXRGanoderic Acid ANeuroinflammation

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