心肌细胞受损是诸多心脏疾病的起始与终归。受损心肌细胞发生能量代谢障碍并重构是其受损的关键。受损心肌中的线粒体自噬失控，过度或不足分别导致的心肌细胞“能量饥饿”和“氧化应激”是发生心肌细胞代谢重构的关键。基于“益气活血”法指导下的芪参益气方在临床上对受损心肌具有肯定的保护作用，其机制是否涉及维持线粒体自噬稳态，改善心肌能量代谢重构是值得研究的科学问题。本研究拟采用在体实验和离体实验相结合的方法，以压力超负荷小鼠代谢重构模型以及原代心肌损伤模型为研究对象，从经典的PINK1/Parkin信号通路为切入点，从心肌细胞线粒体自噬现象的观察、ATP酶活力测定、ROS的产生、心肌细胞凋亡等诸多角度探索该途径介导的线粒体自噬平衡的机制以及芪参益气方及其有效单体的干预作用。

Cardiomyocyte damage is the beginning and ending of many heart diseases. In the damaged cardiomyocytes, the occurrence of metabolic remodeling and structural remodeling are the main cause of the damage. The imbalance of mitochondrial autophagy in damaged myocardium induced "energy starvation" or "oxidative stress", which plays a key role in cardiomyocyte metabolic remodeling. Based on the “Benefiting qi and activating blood circulation” method, Qishenyiqi have a positive effects on cardiomyocyte protection in many clinical studies. However, whether the mechanism involves in mitochondrial autophagy and metabolic remodeling remain unclear. Our study have both in vivo and in vitro part, use metabolic remodeling mice model and primary myocardial injury model. The mitochondrial autophagy mechanism mediated by PINK1/Parkin pathway was explored from the observation of mitochondrial autophagy, ATPase activity, ROS production, cardiomyocyte apoptosis and so on. The intervention effect of Qishenqiqi and its monomer also need observe.