Microglia activation, classification and microglia-mediated neuroinflammatory modulators in subarachnoid hemorrhage.

Subarachnoid hemorrhage is a devastating disease with significant mortality and morbidity, despite advances in treating cerebral aneurysms. There has been recent progress in the intensive care management and monitoring of patients with subarachnoid hemorrhage, but the results remain unsatisfactory. Microglia, the resident immune cells of the brain, are increasingly recognized as playing a significant role in neurological diseases, including subarachnoid hemorrhage.

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.

The Time Course of Cognitive Deficits in Experimental Subarachnoid Hemorrhage.

Subarachnoid hemorrhage (SAH) is a devastating stroke type. Approximately 50% of survivors suffer from the permanent disability, caused by the cognitive deficits. To enrich the pre-clinical research on the neurological deficits after SAH, we investigate the temporal cognitive deficits and the longitudinal course of cognitive recovery in endovascular perforation SAH murine model.

Baicalein enhances the effect of low dose Levodopa on the gait deficits and protects dopaminergic neurons in experimental Parkinsonism.

Parkinson's Disease (PD) is the second most common neurodegenerative disease with the clinical characteristics of gait deficits. The classical symptomatic treatment for PD is Levodopa (L-DOPA) which brings a plethora of side effects and dosage problems in a prolonged drug regimen. Baicalein is a flavonoid extracted from Scutellaria baicalensis Georgi with the properties of neuroprotection.