Background <p>Kawasaki disease (KD) is an acute, self-limiting systemic vasculitis of unknown etiology, which often involves the coronary arteries, leading to severe complications such as myocardial injury (MI). It aimed to explore the mechanism of action of Resveratrol (RES) on MI induced by KD in rats based on the Nrf2/HO-1 pathway.&#xa0;</p> Methods <p>Thirty-six rats were randomly grouped: control, model, RES intervention, Nrf2 inhibitor + RES intervention groups (CG, MG, RG, IRG). The KD rat model was established. After modeling, RES was administered to the RG via intraperitoneal injection, while sterile saline was injected into the CG and MG. Cardiac function, inflammatory factors in myocardial tissue, and related proteins was examined.</p> Results <p>As against the MG, the left ventricular end-diastolic diameter (LVEDd) and left ventricular end-systolic diameter (LVESd) were visibly reduced, while left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were visibly increased in the RG; The levels of inflammatory factors in the RG were visibly decreased but still higher relative to the CG; The relative expression (RE) of Nrf2 and HO-1 in the RG was visibly increased but still lower relative to the CG; In contrast to the MG, the RE of Bcl2 was visibly higher, while the RE of Bax was visibly lower in the RG (<i>P &lt;</i> 0.05); Compared with the RG, the RE of Nrf2 in the nuclear protein of the IRG was significantly decreased to (0.41 ± 0.03) (<i>P</i> &lt; 0.05).</p> Conclusion <p>RES can improve MI and cardiac dysfunction in KD rats by activating the Nrf2/HO-1 pathway, inhibiting inflammatory response and cell apoptosis, providing theoretical and experimental evidence for its application.</p>