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基于微小RNA 200a甲基化途径，皂苷改善冠心病中的血管生成

Saponins Improve Angiogenesis in Coronary Heart Disease Based on the microRNA 200a Methylation Pathway.

作者信息

Wang Jie, Dong Yan, Li Zhaoling, Zhang Yun, Liu Lanchun, Yang Guang, Liu Yongmei, Li Jun, Duan Lian

机构信息

Department of Cardiology, Guang Anmen Hospital, Beijing, People's Republic of China.

出版信息

Drug Des Devel Ther. 2024 Dec 18;18:6075-6087. doi: 10.2147/DDDT.S488036. eCollection 2024.

DOI:10.2147/DDDT.S488036
PMID:39711876
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11663385/
Abstract

BACKGROUND

Improving angiogenesis in the ischemic myocardium is a therapeutic strategy for preventing, reducing, and repairing myocardial injury of coronary artery disease (CAD). saponins (PNS) have been widely used in the clinical treatment of cardiovascular diseases, demonstrating excellent efficacy, and can potentially improve angiogenesis in the ischemic myocardium. However, the effects of PNS on angiogenesis and its underlying mechanism of action remain unclear.

PURPOSE

In this study, we aimed to evaluate the role of PNS in improving angiogenesis after myocardial infarction (MI) and explain the mechanism of PNS in improving angiogenesis in CAD from an epigenetic perspective.

STUDY DESIGN

The MI rat model was established by ligating the left anterior descending coronary artery permanently. The in vitro model comprised hypoxic human coronary artery endothelial cells (HCEACs). The mice and cells were then treated with PNS.

METHODS

Blood tests, histomorphology, polymerase chain reaction, enzyme-linked immunosorbent assay, Western blotting, and MassARRAY targeted methylation detection analyses were conducted in vivo and in vitro to investigate the potential mechanisms of PNS.

RESULTS

Oral PNS significantly improved myocardial injury and activated angiogenesis in MI rats. DNA methylation analysis in vitro revealed that PNS decreased the hypermethylation of microRNA 200a (miR200a). PNS improved angiogenesis in hypoxic human coronary artery endothelial cells (HCEACs) by regulating the vascular endothelial growth factor (VEGF) pathway.

CONCLUSION

Our research shows that PNS can improve angiogenesis in rats with MI and hypoxic HCEACs and affect the level of miR200a promoter methylation and miR200a and VEGF molecular pathways.

摘要

背景

改善缺血心肌中的血管生成是预防、减轻和修复冠状动脉疾病（CAD）心肌损伤的一种治疗策略。人参皂苷（PNS）已广泛应用于心血管疾病的临床治疗，疗效显著，且可能改善缺血心肌中的血管生成。然而，PNS对血管生成的影响及其潜在作用机制仍不清楚。

目的

在本研究中，我们旨在评估PNS在心肌梗死（MI）后改善血管生成中的作用，并从表观遗传学角度解释PNS改善CAD中血管生成的机制。

研究设计

通过永久性结扎左冠状动脉前降支建立MI大鼠模型。体外模型包括缺氧的人冠状动脉内皮细胞（HCEACs）。然后用PNS处理小鼠和细胞。

方法

在体内和体外进行血液检测、组织形态学、聚合酶链反应、酶联免疫吸附测定、蛋白质印迹和MassARRAY靶向甲基化检测分析，以研究PNS的潜在机制。

结果

口服PNS可显著改善MI大鼠的心肌损伤并激活血管生成。体外DNA甲基化分析显示，PNS降低了微小RNA 200a（miR200a）的高甲基化。PNS通过调节血管内皮生长因子（VEGF）途径改善缺氧的人冠状动脉内皮细胞（HCEACs）中的血管生成。

结论

我们的研究表明，PNS可改善MI大鼠和缺氧HCEACs中的血管生成，并影响miR200a启动子甲基化水平以及miR200a和VEGF分子途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/6a990da32835/DDDT-18-6075-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/8e7c2bb7e14c/DDDT-18-6075-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/fa213727b84c/DDDT-18-6075-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/c915aad9b091/DDDT-18-6075-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/97d99f32891d/DDDT-18-6075-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/f24819a860e5/DDDT-18-6075-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/6a990da32835/DDDT-18-6075-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/8e7c2bb7e14c/DDDT-18-6075-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/fa213727b84c/DDDT-18-6075-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/c915aad9b091/DDDT-18-6075-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/97d99f32891d/DDDT-18-6075-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/f24819a860e5/DDDT-18-6075-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42da/11663385/6a990da32835/DDDT-18-6075-g0006.jpg

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Panax notoginseng saponins promote endothelial progenitor cell angiogenesis via the Wnt/β-catenin pathway.
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Increasing heart vascularisation after myocardial infarction using brain natriuretic peptide stimulation of endothelial and WT1 epicardial cells.利用脑钠肽刺激内皮细胞和 WT1 心外膜细胞增加心肌梗死后的心脏血管生成。
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