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P2X7 Receptor Inhibition Mitigates Microglial Activation, Neuroinflammation, and Secondary Thalamic Damage After

Xiaomei Wu1, Ming Gong1, Linhui Peng1

  • 1Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China.

Molecular Neurobiology
|January 28, 2026
PubMed

Insights

Inhibition of the P2X7 receptor (P2X7R) reduces secondary brain damage after ischemic stroke. Blocking P2X7R with Brilliant Blue G (BBG) suppressed neuroinflammation and neuronal loss, improving outcomes.

Area of Science:

  • Neuroscience
  • Neuroinflammation
  • Stroke Research

Background:

  • Secondary brain damage post-stroke worsens outcomes.
  • Microglial activation and P2X7 receptor (P2X7R) are key in neuroinflammation.
  • Mechanisms of secondary damage are not fully understood.

Purpose of the Study:

  • Investigate P2X7R's role in secondary damage in the thalamus after stroke.
  • Assess the therapeutic potential of P2X7R inhibition.

Main Methods:

  • Used a distal middle cerebral artery occlusion (dMCAO) rat model.
  • Analyzed microglial activation, P2X7R expression, and neuronal loss.
  • Inhibited P2X7R with Brilliant Blue G (BBG).
  • Performed molecular dynamics simulations and transcriptome sequencing.

Main Results:

  • Elevated P2X7R expression and microglial activation in the thalamus correlated with neuronal loss.
  • BBG treatment reduced microglial activation, NLRP3 inflammasome activation, and neuronal damage.
  • BBG improved neurological function and altered calcium and cAMP signaling pathways.

Conclusions:

  • P2X7R is a critical driver of neuroinflammation and secondary damage post-stroke.
  • P2X7R inhibition is a promising therapeutic strategy for stroke recovery.
Keywords:
Brilliant Blue GIschemic strokeMicroglial activationNLRP3 inflammasomeP2X7 receptor (P2X7R)Secondary damage

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