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STING Mediates Microglial Polarization to Promote Neuroinflammation in Epilepsy-Related Cognitive Dysfunction.

Hongmei Yang1,2, Weina Wang1,2, Xiang Liu1,2

  • 1Department of Neurology, The Affiliated Hospital of Guizhou Medical University, 28 Guiyi Street, Guiyang, 550001, China.

Neurochemical Research
|March 25, 2026
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Summary

This study reveals that the stimulator of interferon genes (STING) pathway drives neuroinflammation and cognitive deficits in epilepsy. Inhibiting STING shows therapeutic potential by reducing inflammation and improving memory in epilepsy models.

Keywords:
Cognitive dysfunctionEpilepsyMicrogliaNeuroinflammationSTING pathwayTBK1/NF-κB signaling

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Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Epilepsy is a neurological disorder with recurrent seizures and cognitive deficits, often linked to neuroinflammation.
  • The stimulator of interferon genes (STING) pathway's role in epilepsy-related cognitive dysfunction is not well understood.
  • Microglia-mediated immune responses are crucial in epileptogenesis.

Purpose of the Study:

  • To investigate the function of the STING pathway in epilepsy pathology.
  • To explore the therapeutic potential of targeting the STING pathway for epilepsy-related cognitive dysfunction.

Main Methods:

  • Lithium chloride-pilocarpine-induced status epilepticus (SE) in adult male Sprague-Dawley rats.
  • Assessment of hippocampal STING expression temporal dynamics post-SE.
  • Treatment with C-176, a STING inhibitor, and evaluation of seizure severity, cognitive function (Morris water maze), neuroinflammation markers, microglial polarization, and neuronal damage.

Main Results:

  • Hippocampal STING expression peaked 7 days after SE, correlating with cytosolic double-stranded DNA (dsDNA) and M1 pro-inflammatory microglia.
  • C-176 treatment inhibited STING, reduced key inflammatory signaling molecules (p-TBK1, p-NF-κB p65), and decreased pro-inflammatory cytokines.
  • C-176 treatment promoted M1 to M2 microglial repolarization, attenuated neuronal damage, and significantly improved learning and memory in SE rats.

Conclusions:

  • Status epilepticus activates the STING pathway in microglia, leading to neuroinflammation and cognitive dysfunction via the TBK1/NF-κB axis.
  • Inhibition of STING alleviates epilepsy-induced cognitive deficits by modulating microglial polarization and reducing neuroinflammation.
  • The STING pathway represents a promising therapeutic target for treating cognitive dysfunction associated with epilepsy.