首页|期刊导航|中医杂志（英文版）|Matrine alleviates coronary microvascular dysfunction in ischemia with non-obstructive coronary artery disease mice induced by advanced glycation end products via inhibition of the reactive oxygen species-mediated endoplasmic reticulum stress in cardiac microvascular endothelial cells
Matrine alleviates coronary microvascular dysfunction in ischemia with non-obstructive coronary artery disease mice induced by advanced glycation end products via inhibition of the reactive oxygen species-mediated endoplasmic reticulum stress in cardiac microvascular endothelial cells
中医杂志（英文版）2025，Vol.45Issue(3)：473-484,12.
中医杂志（英文版）2025，Vol.45Issue(3)：473-484,12.DOI:10.19852/j.cnki.jtcm.2025.03.006
Matrine alleviates coronary microvascular dysfunction in ischemia with non-obstructive coronary artery disease mice induced by advanced glycation end products via inhibition of the reactive oxygen species-mediated endoplasmic reticulum stress in cardiac microvascular endothelial cells
摘要
Abstract
OBJECTIVE:To investigate the protective effect of matrine on coronary microvascular dysfunction(CMD)induced by advanced glycation end products(AGEs)in a mouse model of ischemia with non-obstructive coronary artery disease(INOCA),with a focus on the underlying mechanisms,particularly the endoplasmic reticulum(ER)stress protein kinase R-like ER kinase(PERK)/nuclear factor of activated T-cells(NFAT)signaling pathway. METHODS:An INOCA model was established in mice,and CMD was induced by peritoneal injections of AGEs.Matrine was administered daily via intraperitoneal injections.Coronary microcirculation was evaluated using coronary flow velocity reserve(CFVR),and cardiac microvascular endothelial cells(CMECs)were isolated for assessment of apoptosis,inflammation,oxidative stress,and microthrombosis.Markers of ER stress and the PERK/NFAT pathway were examined through immunoblotting,immunofluorescence,and enzymatic assays.The effect of matrine were further evaluated in CMECs treated with AGEs and the PERK agonist. RESULTS:Matrine treatment significantly improved CFVR and reduced CMD in AGEs-exposed INOCA mice.In CMECs,matrine attenuated AGEs-induced apoptosis,inflammation,and microthrombosis.It also suppressed intracellular reactive oxygen species(ROS)generation,ER stress markers,and PERK/NFAT signaling.Matrine's effects were concentration-dependent and partially reversed by the PERK agonist,confirming its action through the ER stress pathway.No significant toxicities were observed with matrine administration. CONCLUSION:Matrine attenuates AGEs-induced CMD in INOCA by suppressing the ROS-mediated ER stress PERK/NFAT signaling pathway in CMECs.This study highlights matrine's potential as a therapeutic agent for CMD in diabetic cardiovascular complications.关键词
glycation end products,advanced/matrine/endoplasmic reticulum stress/coronary microvascular dysfunction/cardiac microvascular endothelial cellsKey words
glycation end products,advanced/matrine/endoplasmic reticulum stress/coronary microvascular dysfunction/cardiac microvascular endothelial cells引用本文复制引用
..Matrine alleviates coronary microvascular dysfunction in ischemia with non-obstructive coronary artery disease mice induced by advanced glycation end products via inhibition of the reactive oxygen species-mediated endoplasmic reticulum stress in cardiac microvascular endothelial cells[J].中医杂志（英文版）,2025,45(3):473-484,12.基金项目
Supported by National Natural Scientific Foundation of China:Mechanisms of Macrophage-Mediated Vascular Smooth Muscle Cells Phenotypic Conversion in Advanced Glycation End Products-induced Atherosclerosis and Therapeutic Effects of Targeted Gene Silencing(82070858),Youth Scientific Research and Innovation Team Program of Shaanxi Province:Diabetes-Related Atherosclerosis Basic Research and Application Research Team(2022-SLRH-LJ-014) （82070858）
