Inhibition of neutrophil extracellular traps alleviates blood-brain barrier disruption and cognitive dysfunction via Wnt3/β-catenin/TCF4 signaling in sepsis-associated encephalopathy.

ABSTRACT:

Background

Neutrophils and neutrophil extracellular traps (NETs) have been identified as crucial contributors in several neuroinflammatory models, such as stroke and traumatic brain injury, but their role in sepsis-associated encephalopathy (SAE) has not been thoroughly investigated.

Methods

In this study, we established an SAE model using cecal ligation puncture (CLP) surgery to examine neutrophil infiltration and NETs formation. A protein arginine deiminase 4 (PAD4) inhibitor, GSK484, was employed to suppress NETs release. To assess changes in hippocampal gene expression induced by GSK484 treatment in CLP mice, we utilized RNA sequencing (RNA-Seq) combined with bioinformatics analysis. Additionally, the Elisa, cognitive function test, western bolt and immunofluorescence st

SUBMITTER: Yue J 

PROVIDER: S-EPMC11917101 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature