炎症反应贯穿于心肌缺血再灌注(I/R)损伤的全过程，被视为损害心肌的关键中介环节。我们前期工作证实抗炎是活血化瘀类中药对I/R心肌发挥保护作用的机制之一。AMPK、KATP、NF-κB三种蛋白质在心肌缺血再灌注损伤及炎症反应中各自具有重要作用，最新文献显示，它们两两之间有着一定的联系，但目前未有研究I/R中三者上下游关系及中药对三者之间联系的调控作用的报道。本项目拟从AMPK-KATP-NF-κB信号通路角度探讨三七总皂苷(PNS)抗心肌缺血再灌注引起的炎症反应的作用机制，运用药理学方法，采用膜片钳、Elisa、western blot、实时荧光定量PCR、核蛋白提取、EMSA等技术，从整体和细胞两个水平展开研究，解析这三种蛋白质组成的通路在PNS抗I/R心肌炎症反应中的变化和作用。本研究将为PNS的抗心肌I/R损伤作用增加新的靶点，也为临床应用PNS防治心肌I/R损伤提供理论与实验依据。

Inflammatory response is a crucial mechanism in myocardial ischemia-reperfusion (I/R) injury, regarded as the key link to myocardial damage. We confirmed that anti-inflammatory response is one of the cardioprotection mechanisms of tradition Chinese medicine(TCM), which can activate blood circulation and remove stasis, to against I/R injury previously. AMPK, KATP, NF-κB play important roles in myocardial ischemia-reperfusion injury and inflammation respectively. The latest reports showed that there were interesting links between two of them, but the relation in the three and the regulation of TCM on them remain unknown. In this project, molecular mechanisms of panax notoginseng saponins(PNS) against myocardial ischemia reperfusion and inflammatory response will be investigated based on the AMPK-KATP-NF-κB signal pathway. The changes and relations of these three proteins in cardioprotection of PNS will be observed from in vivo and in vitro(cell) levels by pharmacological methods, patch clamp, Elisa and western blot, real-time fluorescent quantitative PCR, nucleoprotein extraction and EMSA technology. This study will provide new targets of PNS against inflammatory response induced by myocardial I/R injury, and provide theoretical and experimental bases for clinical application in prevention and regulation myocardial I/R injury also.