To investigate the effects of electroacupuncture（EA）preconditioning on myocardial ischemia-reperfusion injury（MIRI）and its regulation of the inflammatory response through the mTOR/NLRP3 signaling pathway.

Seventy SD rats were randomly divided into five groups：sham operation group，model group，EA group，EA+saline group and EA+mTOR agonists（EA+MHY1485）group，with 14 rats in each group. After the intervention，it evaluated cardiac function by measuring the left ventricular ejection fraction（LVEF）and left ventricular fraction shortening（LVFS）. Additionally，it performed hematoxylin-eosin（HE）staining to observe histopathological changes in the myocardium. The levels of tumor necrosis factor-α（TNF-α）in myocardial tissue were measured using an enzyme-linked immunosorbent assay（ELISA）. Furthermore，it assessed the gene expression levels of apoptosis-associated speck-like protein containing a CARD（ASC），cysteinyl aspartate specific proteinase-1（Caspase-1），interleukin-1β（IL-1β）and interleukin-18（IL-18）in cardiac tissue using quantitative polymerase chain reaction（RT-qPCR）. Finally，it analyzed the protein expression levels of mammalian target of rapamycin（mTOR），NOD-like receptor thermal protein domain associated protein 3（NLRP3）and nuclear factor kappa-B（NF-κB）by Western blotting.

Compared to the sham operation group，the rats in the model group showed decreased values of LVFS and LVEF（P<0.05）. Myocardial tissue exhibited muscle fiber rupture，blurred structure and a significant infiltration of inflammatory cells. Additionally，the TNF-αlevel in the myocardial tissue increased（P<0.05）. The relative gene expression levels of Caspase-1，ASC，IL-1βand IL-18 were significantly increased（P<0.05），along with increased protein expression levels of mTOR，NLRP3 and NF-κB. In contrast，the rats in the EA group showed increased FSand EF values（P<0.05）. The myocardial tissue structure improved，inflammatory cell infiltration decreased and the expression of TNF-αin the myocardial tissue decreased（P<0.05）. The relative expression levels of Caspase-1，ASC，IL-1βand IL-18 genes also decreased（P<0.05），as well as the protein expressions of mTOR，NLRP3 and NF-κB（P<0.05）. However，compared to the EA+saline group，the EA+MHY1485 group showed worsened rats myocardial tissue，increased TNF-αlevel in the myocardial tissue（P<0.05），increased relative expression levels of Caspase-1，ASC，IL-1βand IL-18 genes（P<0.05），and increased protein expression levels of mTOR，NLRP3 and NF-κB（P<0.05）.

The mTOR agonist MHY1485 can weaken the protective effect of electricity against myocardial tissue damage in MIRI rats，and EA pretreatment can reduce the inflammatory response of MIRI rat myocardial cells，thereby improving myocardial tissue damage caused by ischemia-reperfusion. Therefore，it is inferred that the mechanism of EA pretreatment to improve MIRI injury in rats may be related to the mTOR/NLRP3 signaling pathway.