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Triggering Reactive Gliosis In Vivo by a Forebrain Stab Injury
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Neutrophil Extracellular Traps Regulate Surgical Brain Injury by Activating the cGAS-STING Pathway.

Bingbing Li1, Lixia Xu1,2, Zhengang Wang1

  • 1Clinical College of Neurology, Neurosurgery and Neurorehabilitation, Tianjin Medical University, Tianjin, 300070, China.

Cellular and Molecular Neurobiology
|April 18, 2024
PubMed
Summary

Surgical brain injury triggers neutrophil extracellular traps (NETs), worsening brain damage. Inhibiting NETs or using vitamin C shows promise for treating surgical brain injury and improving neurological function.

Keywords:
Neutrophil extracellular trapsSTINGSurgical brain injuryVitamin CcGAS

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Area of Science:

  • Neuroscience
  • Immunology
  • Surgical Pathology

Background:

  • Surgical brain injury (SBI) pathophysiology is poorly understood, necessitating new therapeutic approaches.
  • Neutrophil extracellular traps (NETs) have emerged as a potential factor in central nervous system diseases.

Purpose of the Study:

  • To investigate the role of NETs in SBI and explore potential therapeutic interventions.
  • To elucidate the molecular mechanisms linking NETs to SBI pathology.

Main Methods:

  • SBI was induced in a rat model.
  • Presence and effects of NETs were analyzed in circulation and brain tissue.
  • Pharmacological inhibition of NET formation (PAD inhibitor) and disruption (DNase I) were employed.
  • The cyclic guanosine monophosphate-adenosine monophosphate synthase stimulator of interferon genes (cGAS-STING) pathway activation was assessed.
  • High-dose vitamin C was tested for its effect on NET formation.

Main Results:

  • NETs were detected in rats following SBI, correlating with neuroinflammation, edema, and neuronal death.
  • Inhibition or disruption of NETs ameliorated SBI-induced damage and improved neurological recovery.
  • SBI activated the cGAS-STING pathway, and its inhibition was protective.
  • DNase I suppressed cGAS-STING activation, an effect reversed by cGAMP, indicating NETs act via this pathway.
  • High-dose vitamin C inhibited NET formation post-SBI.

Conclusions:

  • NETs play a significant role in the pathophysiology of SBI, exacerbating neurological damage.
  • Targeting NETs, potentially through DNase I or vitamin C, offers a novel therapeutic strategy for SBI.
  • The cGAS-STING pathway is implicated in NET-mediated SBI pathogenesis.