Abstract： Aim To explore the effects and mechanism of simvastatin on the myocardium of rats with Kawasaki disease.Methods SD male rats were randomly divided into control group,model group and simvastatin group,and the rat Kawasaki disease myocardial injury model was constructed by using the extract of Bacillus cereus in the two groups except the control group.The effects of simvastatin on cardiac function and myocardial structure were observed by cardiac ultrasound and histological sections.Serum myo-cardial injury indicators and levels of inflammatory factors in myocardial tissue in each group were detected by ELISA kits.The ex-pression of apoptosis-related proteins,the high mobility group protein B1(HMGB1)/receptor for advanced glycosylation end products(RAGE)pathway-related proteins were detected by immunoblotting in rat myocardial tissues.Results Compared with the control group,the levels of cardiac function indicators and the expression of anti-apoptotic protein B-cell lymphoma 2(Bcl-2)in the model group significantly were decreased,while the infiltration of inflammatory cells in myocardial tissue were increased,Inflammatory cyto-kine levels,expression of pro-apoptotic protein Bcl-2 associated X protein and activated Caspase-3,HMGB1/RAGE pathway protein were increased(P＜0.05).Compared with the model group,the above indicators in the simvastatin group were significantly reversed(P＜0.05).Conclusion Simvastatin can inhibit myocardial damage caused by Kawasaki disease in rats,and its mechanism may be related to the inhibition of the HMGB1/RAGE signaling pathway.