In this study, the cerebral I/R injury models of C57 and caspase-1 gene knockout (Cas-1 ko) mice were established, and the neurological deficit scores, cerebral infarction area, pyroptosis index, and the expression of NLRP3/caspase-1/IL-1β were analyzed to explore the mechanism of EA on nerve cell protection after cerebral ischemia/reperfusion. The gene discussed is NLRP3; the disease is brain infarction.