Objective The study was designed to ascertain whether miR-223-3P protect the myocardium through inhibiting activation of NLRP3（NLR family pyrin domain containing 3） inflammasome, and the underlying mechanisms. Methods Mouse cardiomyoctes H9c2 were cultured in vitro, an cell injury model in H9c2 was induced with indoxyl sulfate (IS).Grouped according to different experimental contents. Cardiomyocytes H9c2 vitality was measured by CCK8 method. Protein expression levels was analyzed by Western blot. miR-223-3P and caspase-1 mRNA expression levels was analyzed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Biological database and the luciferase reporter assay evaluated the interaction between NLRP3 and miR-223-3p. Enzyme linked immunosorbent assay (ELISA) measured IL-1β expression. Results Compared with the Blank group and negative control group, the cell activity decreased，and miR-223-3p levels were reduced(P＜0.05). miR-223-3p can target to bind NLRP3 and negatively regulate NLRP3 expression. Overexpression of miR-223-3p enhanced H9c2 cell viability, and downregulated the expression levels of caspase-1 and IL-1β(P＜0.05)，but the overexpression of NLRP3 reversed these findings. Conclusion In the cardiomyoctes H9c2 injury model，miR-223-3p suppressed inflammation and enhanced cell viability through NLRP3 inflammasome pathway.