The expression of miR-200a was inhibited due to H2O2 stress in MI cardiac tissues; however, the overexpressing of miR-200a could protect cells from death by regulating the Keap1/Nrf2 and β-catenin signal transduction pathways, as well as by reducing levels of IL-1β, IL-6 and TNFα. The gene discussed is IL1B; the disease is myocardial infarction.