NLRP3炎性小体激活诱发的炎症反应是心肌缺血再灌注损伤(MIRI)重要机制，最新研究发现激酶NEK7是介导NLRP3炎性小体激活的关键蛋白。灯盏乙素临床应用广泛，对缺血性心肌病疗效显著，但其作用机制还未完全阐明。前期实验发现缺血再灌注可增加心肌NEK7的表达，并且灯盏乙素对其具有调控作用，提示其可能是介导心肌炎性损伤的重要蛋白。本项目拟在此基础上，采用细胞和动物水平制备心肌缺血再灌注损伤模型，以炎症反应及细胞凋亡为切入点，通过化学抑制剂及RNA干扰技术探索NEK7、NLRP3以及细胞凋亡中相关蛋白的变化，揭示NEK7/NLRP3在MIRI中的作用及灯盏乙素心肌保护机制。本研究为探寻抗MIRI药物提供了新的靶点与思路，并对提高灯盏乙素的临床价值及其二次开发提供理论基础。

The inflammatory response induced by the activation of NLRP3 inflammasome is an important mechanism of myocardial ischemia/ reperfusion injury (MIRI). The latest research found that kinase NEK7 was a key protein which mediated the NLRP3 activation. Scutellarin is widely used in clinic for ischemic cardiomyopathy, which has significantly curative effect. However, its mechanism has not been fully elucidated. Our previous studies have demonstrated that ischemia/ reperfusion could increase the protein expression of NEK7 in myocardium and scutellarin has regulatory effect on it, which suggested that it may be an important protein mediated injury of myocarditis. This project is based on myocardial ischemia/ reperfusion injury model in cellular and animal. Use inflammation and apoptosis as the breakthrough point. The aim is to explore the changes of NEK7, NLRP3 and apoptosis related proteins through chemical inhibitors and RNA interference technology. Reveal the role of NEK7/NLRP3 in MIRI and the mechanism of myocardial protection of Scutellarin. This study provides a new target and ideas for the research of anti-MIRI drugs, and provides theoretical basis for the improvement of the clinical value and the two development of scutellarin.