动脉粥样硬化易损斑块是急性心血管事件的关键病理基础，铁死亡是一种新型的细胞死亡模式，巨噬细胞铁死亡在易损斑块的形成和破裂中扮演着重要角色，FSP1/CoQ10/NAD(P)H是调控铁死亡的全新信号通路。清心解瘀方是在“瘀毒”理论指导下，由陈可冀院士经验方愈梗通瘀汤化裁而来的活血解毒有效复方，网络药理学研究发现，调控巨噬细胞铁死亡是其稳定易损斑块的重要潜在途径，但具体效应机制尚不明晰。因此提出假说：清心解瘀方可调控FSP1/CoQ10/NAD(P)H信号通路，抑制巨噬细胞铁死亡的发生，减轻氧化应激和炎症反应，从而发挥稳定易损斑块的作用。本项目拟体内与体外实验相结合，探索清心解瘀方稳定易损斑块的效应与FSP1/CoQ10/NAD(P)H通路介导的巨噬细胞铁死亡之间的关系，阐明清心解瘀方调控巨噬细胞铁死亡稳定易损斑块的效应机制，为活血解毒稳定易损斑块提供新的科学依据，丰富“瘀毒”理论科学内涵。

Atherosclerotic vulnerable plaque is the key pathological basis for acute cardiovascular events. Ferroptosis is a new cell death form. Macrophage ferroptosis plays an important role in the formation and rupture of vulnerable plaque. FSP1/CoQ10/NAD(P)H is a novel signaling pathway in regulating ferroptosis. Qingxin Jieyu Formula (QXJYF) is an effective compound for activating blood circulation and detoxicating that developed from Yugeng Tongyu Decoction of academician Keji Chen according to the ‘blood-stasis and toxin’ theory. Network pharmacology research found that regulation of macrophage ferroptosis is an important potential way to stabilize vulnerable plaque. However, the specific mechanism remains unclear. Therefore, we put forward the hypothesis that QXJYF can regulate FSP1/CoQ10/NAD(P)H signaling pathway, inhibit macrophage ferroptosis, alleviate oxidative stress and inflammation, thereby stabilizing atherosclerotic vulnerable plaque. This project aims to explore the relationship between the effect of QXJYF in stabilizing vulnerable plaque and FSP1/CoQ10/NAD(P)H pathway-mediated macrophage ferroptosis through both in-vivo and in-vitro study. Results of this project may elucidate the effect mechanism of QXJYF in regulating macrophage ferroptosis and stabilizing vulnerable plaque. At the same time, it will provide new scientific evidence for activating blood circulation and detoxicating in stabilizing vulnerable plaque, thus enriching scientific connotation of the ‘blood-stasis and toxin’ theory.