Novel role of STAT3 in microglia-dependent neuroinflammation after experimental subarachnoid haemorrhage.

Background And Purpose: Signal transducer and activator of transcription 3 (STAT3) may contribute to the proinflammation in the central nervous system diseases by modulating the microglial responses. Thus, this study was intended to investigate the effect of STAT3 on microglia-dependent neuroinflammation and functional outcome after experimental subarachnoid haemorrhage (SAH).

Methods: The SAH model was established by endovascular perforation in the mouse.

The Dynamics of Microglial Polarization Reveal the Resident Neuroinflammatory Responses After Subarachnoid Hemorrhage.

Neuroinflammation plays a critical role in the pathogenesis of subarachnoid hemorrhage (SAH). Microglia, as the resident immune cells, orchestrate neuroinflammation distinctly in neurological diseases with different polarization statuses. However, microglial polarizations in the neuroinflammatory responses after SAH are not fully understood.