Subarachnoid hemorrhage (SAH), a severe cerebrovascular disorder, is principally instigated by the rupture of an aneurysm.Early brain injury (EBI), which gives rise to neuronal demise, microcirculation impairments, disruption of the blood-brain barrier, cerebral edema, and the activation of oxidative cascades, has been established as the predominant cause of mortality among patients with SAH.These pathophysiological processes hinge on the activation of inflammasomes, specifically the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)and absent in melanoma helmets 2 (AIM2) inflammasomes.
These inflammasomes assume a crucial role in downstream intracellular signaling pathways and hold particular significance within the nervous system.The activation of inflammasomes can be modulated, either by independently regulating these two entities or by influencing their engagement at specific target loci within the pathway, thereby attenuating EBI subsequent to SAH.Although read more certain clinical instances lend credence to this perspective, more in-depth investigations are essential to ascertain the optimal treatment regimen, encompassing dosage, timing, administration route, and frequency.
Consequently, targeting the ensuing early brain injury following SAH represents a potentially efficacious therapeutic approach.