大黄素对重症急性胰腺炎大鼠心肌损伤的干预及作用机制的研究

发布时间：2018-06-07 13:33

本文选题：重症急性胰腺炎 + 心肌损伤　；参考：《辽宁医学院》2013年硕士论文

【摘要】：目的研究大黄素（Emodin）对重症急性胰腺炎（severe acute pancreatitis，SAP）大鼠心肌损伤的干预作用，并探讨其作用机制。方法 32只健康雄性SD（Sprague Dawley）大鼠随机平均分为假手术组（A组），模型组（B组），大黄素治疗组(C组)，大黄素加五羟基葵酸钠（5-hydroxydecanoate,5-HD）治疗组(D组)（5-HD可以特异性阻断心肌mitoKATPC的开启）。为采用5％牛磺胆酸钠胰胆管逆行注射方法建立SAP模型。24小时后,采集标本，用ELISA法测定各组大鼠血清肌钙蛋白I（cardial troponin I,CTnI）、肌酸激酶同工酶（creatine kinase-MB，CK-MB）、肿瘤坏死因子-α（Tumor necrosis factor-α，TNF-α）水平，，全自动生化分析仪测定24小时血清淀粉酶（amylase,AMY）水平，用免疫组化法检测术后24小时各组大鼠心肌Bcl-2、Bax基因水平的表达，用TUNEL法检测各组大鼠心肌细胞凋亡情况，光镜下观察各组大鼠胰腺及心肌组织的病理变化及电镜下观察心肌超微结构改变。结果大黄素治疗组大鼠血清CTnI、CK-MB水平，均低于SAP模型组，但仍高于假手术组，均有统计学意义（p0.05）；大黄素加5-HD治疗组低于SAP模型组，高于大黄素治疗组，差异均有统计学意义（p0.05）。血清TNF-α水平，大黄素治疗组低于SAP组，SAP模型组与大黄素加5-HD治疗组没有显著差异(p0.05)。SAP模型组大鼠血清AMY最高，其次为大黄素加5-HD治疗组、大黄素治疗组、假手术组（p0.05）。大黄素治疗组心肌细胞Bax基因表达低于SAP模型组，高于假手术组(p0.05)。假手术组心肌细胞Bcl-2表达最高，大黄素治疗组、大黄素加5-HD治疗组、SAP模型组依次降低(p0.05)。SAP模型组凋亡指数（apoptotic index，AI）高于其他组，其次为大黄素加5-HD治疗组、大黄素治疗组、假手术组（p0.05）。大黄素治疗组大鼠胰腺及心肌组织病理学、超微结构损害较SAP组大鼠减轻，而SAP组大鼠与大黄素加5-HD治疗组差别不明显。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有可能是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K+通道（Mitochondria sensitivitypotassium channel，mitoKATPC）对抗细胞凋亡而实现的。
[Abstract]:Purpose To study the effect of emodin on myocardial injury in rats with severe acute pancreatitis (SAP) and to explore its mechanism. Method 32 healthy male SD(Sprague Dawley rats were randomly divided into sham-operated group (group A), model group (group B), emodin treatment group (group C), emodin plus sodium pentachloroate (5-hydroxydecanoate 5-HDD) group (group D), which could specifically block the opening of myocardial mitoKATPC. In order to establish SAP model by retrograde injection of 5% sodium taurocholate into pancreatic bile duct, the serum levels of troponin (I(cardial troponin), creatine kinase isoenzyme (creatkinase-MBK), tumor necrosis factor- 伪 Tumor necrosis factor- 伪 (TNF- 伪) in serum of rats in each group were determined by ELISA method. The serum amylase (AMY) level was measured by automatic biochemical analyzer, the expression of Bcl-2Bax-Bax gene in myocardium of rats 24 hours after operation was detected by immunohistochemical method, and the apoptosis of cardiac myocytes in each group was detected by TUNEL method. The pathological changes of pancreas and myocardium were observed under light microscope and ultrastructure of myocardium were observed under electron microscope. Result The serum levels of CK-MB in emodin treatment group were lower than those in SAP model group, but still higher than those in sham operation group (P 0.05), and emodin plus 5-HD treatment group were lower than SAP model group and higher than emodin treatment group (P 0.05). The level of serum TNF- 伪 in the emodin treatment group was lower than that in the SAP group. There was no significant difference between the emodin model group and the emodin plus 5-HD group. The serum AMY level in the SAP model group was the highest, followed by emodin plus 5-HD treatment group, emodin treatment group and sham-operation group (p 0.05). The expression of Bax gene in cardiac myocytes in emodin treated group was lower than that in SAP model group and higher than that in sham operation group. The expression of Bcl-2 in cardiomyocytes of sham operation group was the highest, and that of emodin treatment group, emodin plus 5-HD treatment group and emodin plus 5-HD treatment group was significantly lower than that of other groups, followed by emodin + 5-HD treatment group, emodin treatment group and sham operation group (P 0.05). The histopathology and ultrastructure damage of pancreas and myocardium in the emodin treatment group was less than that in the SAP group, but there was no significant difference between the SAP group and the emodin plus 5-HD group. Conclusion Emodin can attenuate the pathological changes and myocardial injury of SAP. The protective effect of emodin on myocardium may be achieved by inhibiting the production of inflammatory mediators and activating Mitochondria sensitivitypotassium channel Mitochondria sensitivitypotassium channel Mitmito KATPC. it is possible that emodin can inhibit the production of inflammatory mediators and activate Mitochondria sensitivitypotassium channel mito KATPC.
【学位授予单位】：辽宁医学院
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R657.51

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