In traditional Chinese medicine,coronary heart disease falls under the categories of"chest impediment and heart pain"and"true heart pain",with lipid metabolism disorder and the inflammatory response acting as biochemical manifestations of"phlegm and stasis"throughout the disease.The energy metabolism of macrophages is closely related to their immune function and is an important factor in regulating the metabolic disorder and inflammatory responses in coronary heart disease.This article reviews the role of macrophages in the pathophysiology of coronary heart disease.We discuss how these metabolic pathways affect the immune responses of macrophages and influence the disease.We delve into the different modes of macrophage energy metabolism in coronary heart disease,especially the metabolic characteristics and immune regulatory functions of pro-inflammatory M1 and anti-inflammatory M2 macrophages in the syndrome of phlegm and blood stasis.This provides a theoretical guidance for understanding the pathogenic mechanism of the syndrome of phlegm and blood stasis in coronary heart disease and developing new treatment strategies.

Cardiovascular disease presents a serious threat to human life,and oxidative stress has been identified as an important factor affecting the occurrence and development of cardiovascular disease.The construction of reliable animal models of oxidative stress is important for the in-depth study of the pathogenesis of cardiovascular diseases and the development of therapeutic drugs.Zebrafish have often been for research into cardiovascular diseases,due to their advantages of easy reproduction,a short developmental cycle,transparent embryos for easy observation,and a highly homologous cardiovascular genetic background with humans.In this paper,we review the application of the zebrafish oxidative stress model in cardiovascular disease and related research progress,to provide a reference for its further application in cardiovascular disease-related research.

Objective To investigate the function of burdock leaf extract NBY-4 in protecting vascular endothelial cells from oxidative damage.Methods The oxidative damage model of vascular endothelial cells was established with hydrogen peroxide(H2O2).ROS,LDH,SOD,apoptosis rate and the expression of apoptosis were measured;Further test the nuclear transcription factor-κB(NF-κB).Results In the model group,H2O2 increased the apoptosis rate of endothelial cells,increased the ratio of Bax/Bcl-2 and the expression of Caspase-3,promoted the production of ROS and LDH in endothelial cells,and inhibited the level of SOD,resulting in oxidative damage to endothelial cells(P<0.05).NBY-4 could slow down the process of these effects;At the same time,NBY-4 can reduce NF-κB in endothelial cells.Conclusion NBY-4 can inhibit endothelial cell apoptosis and antioxidant damage by NF-κB signaling pathway.

As an effective anticancer drug, the clinical limitation of doxorubicin (Dox) is the time- and dose-dependent cardiotoxicity. Yes-associated protein 1 (YAP1) interacts with transcription factor TEA domain 1 (TEAD1) and plays an important role in cell proliferation and survival. However, the role of YAP1 in Dox-induced cardiomyopathy has not been reported. In this study, the expression of YAP1 was reduced in clinical human failing hearts with dilated cardiomyopathy and Dox-induced