After stroke, under the environmental conditions of excitatory toxicity and oxidative stress, NLRP3 inflammasomes are activated, promoting the cleavage and maturation of Caspase-1 which cleaves and splits gasdermin D (GSDMD) and pro-interleukin-1β, pro-interleukin-18, forming GSDMD-N and IL-1β,IL-18, suggesting microglia activation [110], mediating nerve cell dysfunction and brain edema and ultimately leading to nerve cell death [111, 112]. Here, CASP1 is linked to stroke disorder.