大黄素对重症急性胰腺炎大鼠并发心肌损伤的作用机制

目的研究大黄素对大鼠重症急性胰腺炎severeacutepancreatifis，SAP）合并心肌损伤的作用机制。方法32只sD大鼠随机分为假手术组（A组，8只），模型组（B组，8只），大黄素治疗组（C组，8只），大黄素加五羟基葵酸钠（5-hydmxydecanoate，5-HD）治疗组（D组，8只oSAP模型采用5％牛黄胆酸钠胰胆管逆行注射方法建立。ELISA法测定24h后各组血清CTnI、CK-MB、TNF-α水平，免疫组化检测术后24h心肌Bcl-2、Bax基因的表达水平，TURNEL法测心肌细胞凋亡指数，光镜下观察胰腺及心肌组织病理变化及电镜下观察心肌超微结构。结果CTnI和CK-MB含量，C组分别为（0．43±0．35）mg／L、（10．47±1．08）U／L，均较B组的（4．30±0．35）mg／L、（79．85±6．68）U／L，D组的（4．03±0．18）mg／L、（75．99±2．05）U／L低（P〈0．05）。TNF-α含量，C组为（0．96±0．07）mg／L，较B组（3．79±0．17）mg／L和D组（1．10±0．27）mg／L低（P〉0．05）。Bcl-2表达量，从高到低依次为A组0．28％±0．06％、C组0．28％±0．06％、D组0．21％±0．11％、B组0．10％±0．03％（P〈0．05）。Bax表达量，从高到低依次为B组3．25％±0．37％、D组2．85％±0．30％、C组为1．65％±0．50％、A组0．94％±0．13％（P〈0．05）。细胞凋亡指数，从高到低依次为B组35．30％±2．86％、D组31．6％±3．5％、C组为25．86％±1．32％、A组2．20％±0．82％（P〈0．05）。结论大黄素能减轻SAP的病变程度和心肌损伤，其对心肌的保护作用可能通过抑制炎症介质的产生，激活心肌细胞线粒体膜ATP敏感性对通道对抗细胞凋亡而实现。

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 immunohistochemlcal 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- 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.