Objective：This study aimed to investigate the role of receptor for advanced glycation end products（RAGE）in improving myocardial ischemia and reperfusion after remote ischemic postconditioning. Methods：Thirty-four C57/B6 mice aged 8-9 weeks were randomly divided into six groups：the sham operation group（sham），the FPS-ZM1 control group（FZM1），the ischemia and resperfusion group（IR），the FPS-ZM1 intervention group（FZM1+IR），the RIPostC group（RIPostC+IR）and the RIPostC intervention group（RIPostC+FZM1+IR）. The anterior descending coronary artery was ligated to create myocardial ischemia-reperfusion model of mouse. The left ventricular ejection fraction（LVEF）and left ventricular shortening fraction（LVFS）of mice were detected by mouse cardiac ultrasonography，and the inflammatory factor IL-6，NF-κB P65 protein and RAGE protein were detected by enzyme-linked immunoassay（ELISA）and Western blotting. Results：①RIPostC significantly increased LVEF（P < 0.01）and LVFS（P < 0.01）compared with the I/R group. ②Compared with the IR group，RIPostC significantly reduced the expression of RAGE（P < 0.001）. ③RIPostC significantly reduced the expression of NF-κB P65（P < 0.001）and IL-6（P < 0.001）compared with the I/R group. Conclusion：RIPostC was effective in protecting against myocardial ischemia-reperfusion injury. The cardioprotective effects of RIPostC may be achieved directly by inhibiting the expression of RAGE and thereby reducing the inflammatory response.