ColCaNP treatment significantly reduced the myocardial infarction area by approximately 45%, alleviated myocardial fibrosis, and lowered serum levels of CRP, TNF-α, and IL-1β. It also regulated M1/M2 macrophage polarization, inhibited the TLR4/NFκB/NLRP3 signaling pathway, and significantly suppressed pyroptosis and inflammation, thereby mitigating AMI-induced damage. The gene discussed is IL1B; the disease is myocardial infarction.