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Edaravone Alleviates BV-2 Microglia-Mediated Neuroinflammation Through the PI3K/AKT/ NF-κB Pathway

Li Yang1, Zhaoda Duan1,2, Dongyao Xu1

  • 1School of basic medical science, Kunming Medical University, Kunming, 650500, China.

Advanced Biology
|April 8, 2025
PubMed

Insights

Edaravone (EDA) may treat ischemic stroke by reducing neuroinflammation. This study suggests EDA works by inhibiting microglia activation via the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Ischemic stroke (IS) is a major health concern.
  • Microglia (MG)-mediated neuroinflammation is critical in IS pathogenesis.
  • Targeting MG activation offers potential therapeutic strategies for stroke and neurodegenerative diseases.

Purpose of the Study:

  • To elucidate the anti-inflammatory mechanisms of Edaravone (EDA) in ischemic stroke.
  • To investigate the role of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway in EDA's effects on microglia.

Main Methods:

  • Network pharmacology (NP) analysis to identify potential pathways.
  • In vitro (oxygen-glucose deprivation in BV-2 cells) and in vivo (middle cerebral artery occlusion in mice) models of ischemic stroke.
  • Western blot, immunofluorescence staining, PI3K pathway inhibitor (LY294002), and PI3K overexpression plasmid to analyze molecular changes.

Main Results:

  • Network pharmacology identified the PI3K/Akt pathway as a potential target of EDA in microglia.
  • EDA treatment modulated phosphorylation levels of PI3K/Akt pathway proteins and inflammatory factors in both in vitro and in vivo models.
  • Pharmacological and genetic manipulation of the PI3K pathway confirmed its involvement in EDA's anti-inflammatory effects.

Conclusions:

  • Edaravone (EDA) may exert its anti-inflammatory effects in ischemic stroke by modulating the PI3K/Akt signaling pathway.
  • Inhibition of microglia activation through the PI3K/Akt pathway is a key mechanism for EDA's therapeutic potential.
  • These findings provide a mechanistic basis for EDA's clinical use in ischemic stroke and suggest potential for other neuroinflammatory conditions.
Keywords:
PI3K/Akt signaling pathwayedaravoneinflammationischemic strokemicroglianetwork pharmacology

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