Effect of emodin on severe acute pancreatitis accompanying myocardial damage and its mechanism

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.