稳心丹不同比例配伍对MIRI模型大鼠抗炎机制研究

发布时间：2018-07-09 22:43

本文选题：心肌缺血再灌注损伤 + 稳心丹　；参考：《黑龙江中医药大学》2017年博士论文

【摘要】：目的:探讨稳心丹不同配伍比例对心肌缺血再灌注损伤模型大鼠的心肌保护作用及相关抗炎机制。方法:1.将70只SD大鼠随机分为7组,即模型组、假手术组、预处理组、稳心丹1:1:1组、稳心丹1:2:1组、稳心丹1:1:2组、稳心丹2:1:1组,分别作用于心肌缺血再灌注损伤模型大鼠,检测其对模型大鼠血清CK-MB、cTnI的含量及心肌梗死面积的影响;进行稳心丹配伍比例关系量化考查,选出最优配伍比例组。2.运用透射电镜观察稳心丹对心肌缺血再灌注损伤模型大鼠的心肌超微细结构的影响,免疫组化法检测稳心丹对心肌组织中T-Akt、p-Akt的表达的影响。从而探讨稳心丹抗心肌缺血再灌注损伤的作用机制。3.通过免疫印迹法、免疫组化法检测稳心丹对心肌缺血再灌注损伤模型大鼠心肌组织中NF-κB、COX-2的蛋白分布及表达的影响。4.观察稳心丹对心肌缺血再灌注损伤模型大鼠血清中TNF-α、IL-1β、IL-6、IL-10含量的影响,探讨其抗炎作用机制。结果:1.稳心丹各治疗组均能够明显降低心肌缺血再灌注损伤模型大鼠血清中CK-MB、cTnI含量、使MIRI模型大鼠心肌梗死面积减小,其中稳心丹1:2:1组效果最为显著。2.稳心丹1:2:1组与模型组比较可显著改善心肌缺血再灌注损伤模型大鼠的心肌超微细结构;提高心肌组织p-Akt蛋白表达。3.稳心丹1:2:1组与模型组比较可显著抑制心肌缺血再灌注损伤模型大鼠心肌组织中NF-κB、COX-2的蛋白分布及表达。4.稳心丹1:2:1组与模型组比较可显著降低心肌缺血再灌注损伤模型大鼠血清中TNF-α、IL-1β、IL-6的含量,升高IL-10的含量。结论:1.稳心丹不同配伍比例组均能明显降低心肌缺血再灌注损伤模型大鼠心肌酶CK-MB、cTnI含量,使MIRI模型大鼠心肌梗死面积减小,选出抗心肌缺血再灌注最佳配伍比例组为稳心丹1:2:1组。2.稳心丹通过激活PI3K/Akt信号转导通路,提高心肌组织p-Akt蛋白表达,减少NF-κB、Cox-2蛋白表达,减轻心肌组织损伤程度,发挥心肌保护作用。3.稳心丹通过激活PI3K/Akt信号转导通路,下调炎症因子TNF-α、IL-1β、IL-6表达,并能够促进抑炎因子IL-10释放,进而发挥心肌保护作用。
[Abstract]:Aim: to investigate the protective effect of Wenxindan (WXD) on myocardium in rats with myocardial ischemia reperfusion injury and its related anti-inflammatory mechanism. Method 1: 1. 70 SD rats were randomly divided into 7 groups: model group, sham operation group, preconditioning group, Wenxindan 1:1:1 group, Wanxindan 1:2:1 group, Wanxindan 1:1:2 group and Wenxindan 1:1:2 group. The effect of CK-MBN cTnI on serum and myocardial infarction area in model rats was detected, and the optimal compatibility ratio group was selected by quantitative examination of compatibility ratio of Wanxin Dan. The effects of Wenxindan on the ultrafine structure of myocardium in rats with myocardial ischemia-reperfusion injury were observed by transmission electron microscope, and the expression of T-AktP- Akt in myocardial tissue was detected by immunohistochemical method. So as to explore the mechanism of Wenxin Dan on myocardial ischemia reperfusion injury. 3. The effects of Wenxindan on the protein distribution and expression of NF- 魏 B, COX-2 in myocardial tissue of rats with myocardial ischemia-reperfusion injury were detected by Western blot and immunohistochemistry. To observe the effect of Wenxindan on the content of TNF- 伪, IL-1 尾 and IL-6IL-10 in serum of myocardial ischemia-reperfusion injury model rats, and to explore its anti-inflammatory mechanism. The result is 1: 1. The serum CK-MBN cTnI content in rats with myocardial ischemia-reperfusion injury was significantly decreased in each treatment group, and the myocardial infarction area was decreased in MIRI model rats, among which the effect of Wanxindan 1:2:1 group was the most significant. 2. Compared with the model group, Wenxindan 1:2:1 group could significantly improve the myocardial ultrafine structure and increase the expression of p-Akt protein. 3. Compared with model group, Wenxindan 1:2:1 group could significantly inhibit the distribution and expression of COX-2 protein in myocardial tissue of myocardial ischemia-reperfusion injury model rats. Compared with the model group, Wenxindan 1:2:1 group could significantly reduce the content of TNF- 伪, IL-1 尾, IL-6 and increase the content of IL-10 in the serum of myocardial ischemia-reperfusion injury model rats. Conclusion 1. The content of myocardial enzyme CK-MBN cTnI in rats with myocardial ischemia-reperfusion injury was significantly decreased in the groups of different combinations of Wenxindan, and the myocardial infarction area of MIRI model rats was reduced. The best proportion of anti-myocardial ischemia and reperfusion was chosen as the 1:2:1 group of Wenxindan group. 2. Through activating PI3K / Akt signal transduction pathway, Wanxin Dan can increase the expression of p-Akt protein, decrease the expression of NF- 魏 B, decrease the degree of myocardial injury, and play a protective role in myocardium. Through activating PI3K / Akt signal transduction pathway, Wanxin Dan can down-regulate the expression of inflammatory factor TNF- 伪, IL-1 尾 and IL-6, promote the release of anti-inflammatory factor IL-10, and then play a protective role in myocardium.
【学位授予单位】：黑龙江中医药大学
【学位级别】：博士
【学位授予年份】：2017
【分类号】：R285.5;R-332

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