A literature overview on epilepsy and inflammasome activation

•NLRP1 and NLRP3 inflammasome activation is involved in epilepsy development.•Knockout or knockdown of these molecules improves the symptoms of epilepsy.•Inhibitors of inflammasome complex components can improve the epilepsy symptoms.•Some drugs improve the epilepsy symptoms by affecting inflammasome signaling.•Modification of molecules somehow linked to this pathway is useful in treatment. Epilepsy is one of the most prevalent serious brain disorders worldwide. Accumulating evidence has suggested that inflammation participates in the progression and pathogenesis of epilepsy. During inflammation, a cytosolic multimolecular complex called the "inflammasome" is activated, driving the innate immune response. This inflammatory pathway by sensing various pathogens and molecules from damaged cells and then activation of caspase-1 enzyme initiates inflammatory responses. Activated caspase-1 leads to the proteolytic cleavage of the pro-inflammatory cytokines, interleukin-1β (IL-1β) and interleukin-18 (IL-18), and also induction of an inflammatory programmed cell death termed pyroptosis. NLR family pyrin domain-containing 1 (NLRP1) and NLRP3 are the two best-characterized inflammasome members, and both basic and clinical research has reported their activation during epilepsy. This overview is intended to summarize the current literature concerning NLRP1 and NLRP3 inflammasome activation and epilepsy.