Abstract: Objective To study the effect of emodin on severe acute pancreatitis（SAP） accompanying myocardial damage and its mechanism. Methods Thirty-two male SD rats were randomly divided into sham-operated group（group A）,control group（group B） and emodin treatment group（group C）,and emodin plus 5-hydroxydecanoate（5-HD） treatment group,8 in each group.Twenty-four hours after a SAP model was established by retrograde 5% sodium taurocholate injection into pancreatic duct,serum levels of CTnI,CK-MB and TNF-α and expression levels of Bcl-2 and Bax in myocardial tissue were measured by ELISA and SP immunohistochemical technique,respectively.Apoptosis index of myocardial cells was detected by TUNEL.Ultra-structures of pancreatic and myocardial tissues were observed under light and electron microscopes respectively. Results The serum levels of CTnI,CK-MB and TNF-α were significantly lower in group C than in groups B and D（0.43±0.35） mg/L and（10.47±1.08）U/L vs（4.30±0.35） mg/L and（79.85±6.68） U/L,（4.03±0.18） mg/L and（75.99±2.05） U/L;（0.96±0.07） mg/L vs（3.79±0.17） mg/L and（1.10±0.27） mg/L, P＜0.05).The expression level of Bcl-2 was the highest in group A followed by in groups C,D and B（0.28%±0.06% followed by 0.28%±0.06%,0.21%±0.11% and 0.10%±0.03%,P＜0.05）.The expression level of Bax was the highest in group B followed by in groups D,C and A（3.25%±0.37% followed by 2.85%±0.30%,1.65%±0.50% and 0.94%±0.13%,P＜0.05）.The apoptosis index was the highest in group B followed by in groups D,C and A（35.30%±2.86% followed by 31.60%±3.5%,25.86%±1.32% and 2.20%±0.82%,P＜0.05）. Conclusion Emodin can alleviate lesions and myocardial damage in SAP rats by inhibiting the production of inflammatory mediators,activating the mitochondrial ATP-sensitive potassium channel,and inducing the cell apoptosis.