Our findings demonstrate that DAT enhances cardiomyocyte survival through antioxidant actions mediated by modulation of the NADP+/NADPH ratio, a mechanism that has not been previously explored in our earlier work or in other studies targeting cardiovascular diseases with microbiota‐derived interventions.[5, 6, 22] Additionally, DAT specifically suppresses macrophage proinflammatory activities by reducing IL‐6 production in a redox‐dependent manner, without altering macrophage numbers, highlighting a redox‐dependent mechanism for immune modulation in the context of myocardial I/R injury. This evidence concerns the gene IL6 and cardiovascular disorder.