Abstract
The inflammasome is assembled in response to a wide range of patterns associated with pathogens or damage molecules inpresence of brain injury, they are multiproteic complexes that comprise a sensor, an adapter protein and a zymogenic enzyme thatactivates caspase-1 for secretion of mature proteins of IL-1β and IL-18 that trigger pyroptosis (neuroinflammation-induced celldeath) which is involved in the onset and development of several pathophysiological events. Until now, four inflammasomes havebeen described that recruit the Apoptosis-associated speck-like (ASC) adapter protein to activate caspase-1: NLRP-1, NLRP-3,NLRC4 and AIM2. The activation of the NLRP-3 inflammasomes are mediated by variations in K⁺ concentrations, increasedextracellular ATP and oxidative stress mainly. Because of this, it has been implicated in the pathogenesis of several neurologicaldisorders such as epilepsy; which is a neurological disorder characterized by the presence of spontaneous and a recurrent seizure(SRS) that affects around 70 million people in the world. SRS are generated by the establishment of the epileptome (defined area ofepileptogenesis) triggered by genetic or acquired factors that cause structural and functional modifications, such asneuroinflammation that induces oxidative stress, neuronal loss, reactive gliosis and pathological synaptic reorganization.Neuroinflammation can be preserved during epileptogenesis due activation of the NLRP-3 inflammasome. On the other hand, awide variety of inhibitors have been used to alter the secretion of IL-1β and IL-18, indirect inhibitors of NLRP-3, ASC and caspase-1; however, these only disturb the signaling pathways without directly regulating NLRP-3 and blocked the pathologicalneuroinflammatory response. For this reason, it is important to study the activation and modulation of inflammasomes like NLRP-3in epileptogenic processes to expand the view on neuroinflammation and its possible mechanisms involved in epilepsy.
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