肠道菌群(GM)失调及其代谢物异常导致免疫炎症反应与动脉粥样硬化(AS)密切相关。研究发现GM代谢物短链脂肪酸(SCFAs)可通过巨噬细胞HDACs/mTOR信号通路调控其能量代谢和极化抗AS。清心解瘀方由“瘀毒”理论指导下的陈可冀院士经验方愈梗通瘀汤化裁而来。课题组前期研究发现，清心解瘀方可显著改变ApoE-/-小鼠GM及SCFAs水平，减少AS斑块面积及单核/巨噬细胞表达，降低IL-1β水平，但机制尚不清楚。据此提出假说：清心解瘀方通过GM-SCFAs代谢调控巨噬细胞HDAC3/mTOR信号通路改变其能量代谢和极化，减少促炎因子释放抗AS。本研究拟体内与体外研究相结合，衔接GM-SCFAs和巨噬细胞能量代谢这一前沿热点，探讨清心解瘀方抗AS的效应机制，以期为AS的中医药干预提供新思路，丰富“瘀毒”理论科学内涵，进一步提高AS性心血管病的中医药防治效果。

The dysbiosis of gut microbiota (GM) and its metabolites may lead to a close association of immunoinflammation and atherosclerosis (AS). Short chain fatty acids (SCFAs) are metabolites of GM, which regulate macrophage energy metabolism and polarization, and reduce the inflammatory response by suppressing HDACs/mTOR pathway in macrophages. Qingxin Jieyu Fang (QXJYF) is based on the Academician Chen Ke-ji's experienced formula "Yugeng Tongyu Tang", which is under the guidance of the theory of "blood stasis and toxin". Our previous research found that QXJYF significantly changed the GM and SCFAs levels of high fat diet fed ApoE-/- mice, reduced the plaque area and mononuclear/macrophage expression of AS area, and reduced the IL-1β level. But the mechanism is still unclear. Therefore, our hypothesis is proposed: QXJYF regulates the HDAC3/mTOR signal pathway of macrophages to modulate their energy metabolism and polarization through changing GM and SCFAs metabolism, and reduces the pro-inflammatory cytokines to alleviate AS. The research is proposed to combine in vivo and in vitro research, connecting GM-SCFAs and macrophage energy metabolism and exploring the anti-AS mechanism of QXJYF. Our research may help enrich the scientific connotation of the theory of "blood stasis and toxin", and further improve the prevention and treatment of AS cardiovascular disease by Chinese medicine.