BACKGROUND:The energy metabolism and polarization state of macrophages play a crucial role in the progression of atherosclerosis.Traditional Chinese Medicine(TCM)has shown significant therapeutic potential for prevention and treatment of atherosclerosis by regulating macrophage metabolic pathways.OBJECTIVE:To review the research progress in AMP-activated protein kinase regulation of macrophage energy metabolism and polarization and explore the mechanism of TCM in the prevention and treatment of atherosclerosis.METHODS:A computerized search was conducted on the databases including Web of Science,PubMed,and CNKI,covering relevant literature up to June 2024.The search terms were"AMPK,fatty acid oxidation,macrophage polarization,Traditional Chinese Medicine,atherosclerosis,coronary heart disease"in Chinese and English.A total of 62 articles were finally included for review.RESULTS AND CONCLUSION:The shiftin macrophage energy metabolism from oxidative phosphorylation to glycolysis plays a key role in the progression of atherosclerosis.The activation of AMP-activated protein kinase in macrophages promotes fatty acid oxidation and M2 polarization,exerting anti-inflammatory effects and stabilizing arterial plaques.TCM monomers(such as ginseng,astragalus,and polygonatum)and compounds(such as Huanglian Jiedu Decoction,Yangxin Shumai Granules,and Tiaogan Daozhuo Formula)influence macrophage metabolism and cellular function by regulating the AMP-activated protein kinase pathway and intervening in multiple signaling pathways,such as nuclear factor-κB,peroxisome proliferator-activated receptor γ,and mammalian target of rapamycin,thereby achieving therapeutic effects.Future research should focus on the interactions between AMP-activated protein kinase,metabolism,and polarization pathways,as well as how TCM exerts its therapeutic effects through these pathways,providing new strategies for the treatment of atherosclerosis.

BACKGROUND:The energy metabolism and polarization state of macrophages play a crucial role in the progression of atherosclerosis.Traditional Chinese Medicine(TCM)has shown significant therapeutic potential for prevention and treatment of atherosclerosis by regulating macrophage metabolic pathways.OBJECTIVE:To review the research progress in AMP-activated protein kinase regulation of macrophage energy metabolism and polarization and explore the mechanism of TCM in the prevention and treatment of atherosclerosis.METHODS:A computerized search was conducted on the databases including Web of Science,PubMed,and CNKI,covering relevant literature up to June 2024.The search terms were"AMPK,fatty acid oxidation,macrophage polarization,Traditional Chinese Medicine,atherosclerosis,coronary heart disease"in Chinese and English.A total of 62 articles were finally included for review.RESULTS AND CONCLUSION:The shiftin macrophage energy metabolism from oxidative phosphorylation to glycolysis plays a key role in the progression of atherosclerosis.The activation of AMP-activated protein kinase in macrophages promotes fatty acid oxidation and M2 polarization,exerting anti-inflammatory effects and stabilizing arterial plaques.TCM monomers(such as ginseng,astragalus,and polygonatum)and compounds(such as Huanglian Jiedu Decoction,Yangxin Shumai Granules,and Tiaogan Daozhuo Formula)influence macrophage metabolism and cellular function by regulating the AMP-activated protein kinase pathway and intervening in multiple signaling pathways,such as nuclear factor-κB,peroxisome proliferator-activated receptor γ,and mammalian target of rapamycin,thereby achieving therapeutic effects.Future research should focus on the interactions between AMP-activated protein kinase,metabolism,and polarization pathways,as well as how TCM exerts its therapeutic effects through these pathways,providing new strategies for the treatment of atherosclerosis.

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