Esketamine attenuates traumatic brain injury by modulating STAT3-mediated Glycolysis and immune responses.

ABSTRACT:

Background

Secondary injury following traumatic brain injury (TBI) involves neuroinflammation, immune cell infiltration, and metabolic dysregulation, leading to progressive neurological damage. This study evaluates the potential of esketamine, an NMDA receptor antagonist, to modulate immune responses, inhibit glycolysis, and mitigate secondary brain injury in a TBI mouse model.

Methods

Male C57BL/6J mice were subjected to controlled cortical impact to induce TBI. Mice were treated with esketamine, either alone or combined with the STAT3 activator colivelin, or the glycolysis inhibitor 2-deoxyglucose (2-DG). Neurological function, BBB permeability, immune cell infiltration, macrophage polarization, and glycolytic activity were assessed using immunohistochemistry, flow cytomet

SUBMITTER: Liu Y 

PROVIDER: S-EPMC11889827 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature