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To investigate the effect of propofol pretreatment on microglial pyroptosis in the ischemic penumbra of rats subjected to cerebral ischemia-reperfusion. 90 rats were randomly divided into Sham group, model group, nod-like receptor protein 3 inhibitor group, propofol low dose group and high dose group. Pathological changes in the hippocampal region of the ischemic penumbra of brain tissue were observed by hematoxylin and eosin staining; interleukin-1 beta and interleukin-18 levels were detected in the ischemic penumbra of cerebral tissue by enzyme-linked immunosorbent assay; immunofluorescence double staining was performed to detect the immunopositive co-expression of nod-like receptor protein 3, aspartate specific caspase 1 and ionized calcium adaptor protein 1 in the ischemic penumbra of cerebral tissue. Compared with the model group, the nod-like receptor protein 3 inhibitor group, propofol low dose group and propofol high dose group groups also had significantly lower neurological deficit scores, cerebral infarction volumes, and interleukin-1 beta and interleukin-18 levels, ionized calcium adaptor protein 1/nod-like receptor protein 3, ionized calcium adaptor protein 1/caspase 1 immunopositive co-expression, nod-like receptor protein 3, pro-caspase 1, P10, P20 and interleukin-1 beta protein expressions in the ischemic penumbra were significantly reduced (p<0.05), the pathological damage was improved to various degrees, and the number of nerve cells was increased. The neuroprotective effect of propofol pretreatment on cerebral ischemia-reperfusion injury may be related to the inhibition of microglial pyroptosis mediated by nod-like receptor protein 3 inflammasome. [ABSTRACT FROM AUTHOR]