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淫羊藿苷激活自噬以触发TGFβ1上调并促进EA.hy926人血管内皮细胞中的血管生成。

Icariin activates autophagy to trigger TGFβ1 upregulation and promote angiogenesis in EA.hy926 human vascular endothelial cells.

作者信息

Li Xiaolong, Wen Yujie, Sheng Liyuan, Guo Rui, Zhang Yanli, Shao Longquan

机构信息

Foshan Stomatological Hospital, School of Medicine, Foshan University, Foshan, PR China.

Shenzhen Institute, Peking University, Shenzhen, China.

出版信息

Bioengineered. 2022 Jan;13(1):164-177. doi: 10.1080/21655979.2021.2011637.

DOI:10.1080/21655979.2021.2011637
PMID:34847836
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8805869/
Abstract

Angiogenesis plays an important role in tissue development and repair, and how to regulate angiogenesis effectively is a widely studied problem in the biomedical field. In recent years, the role of autophagy in vascular endothelial cells has attracted extensive attention. Icariin (ICA) is a traditional Chinese medicine that has been proven to have outstanding protective effects on the vascular system and to regulate cellular autophagy effectively. However, at present, it has not been reported whether ICA can affect the angiogenic ability of endothelial cells by affecting autophagy. In this study, we aimed to investigate whether ICA affects the angiogenesis capacity of EA.hy926 human vascular endothelial cells through autophagy and explain the underlying potential mechanisms. First, we determined that ICA at appropriate concentrations has the ability to promote cell migration and angiogenesis using wound healing assays and tube formation assays. Then, at the molecular level, we observed the upregulation of VEGFA, VEGFR2, ANGI, ANGII, and Tie2 mRNA and detected the upregulation of TGFβ1 protein by Western blotting. We also demonstrated that angiogenic concentrations of ICA can effectively activate autophagy. The autophagy inhibitor 3-MA significantly suppressed TGFβ1 expression and tube formation in EA.hy926 cells. Overall, we hope that our studies might help to further understand the effect of ICA on vascular endothelial cells and provide a theoretical basis for future angiogenic applications of ICA.

摘要

血管生成在组织发育和修复中起着重要作用,如何有效调节血管生成是生物医学领域广泛研究的问题。近年来,自噬在血管内皮细胞中的作用引起了广泛关注。淫羊藿苷(ICA)是一种传统中药,已被证明对血管系统具有显著的保护作用,并能有效调节细胞自噬。然而,目前尚未见关于ICA是否能通过影响自噬来影响内皮细胞血管生成能力的报道。在本研究中,我们旨在探讨ICA是否通过自噬影响EA.hy926人血管内皮细胞的血管生成能力,并阐明其潜在机制。首先,我们通过伤口愈合实验和管腔形成实验确定了适当浓度的ICA具有促进细胞迁移和血管生成的能力。然后,在分子水平上,我们通过Western印迹观察到VEGFA、VEGFR2、ANGI、ANGII和Tie2 mRNA的上调,并检测到TGFβ1蛋白的上调。我们还证明了血管生成浓度的ICA能有效激活自噬。自噬抑制剂3-MA显著抑制EA.hy926细胞中TGFβ1的表达和管腔形成。总体而言,我们希望我们的研究有助于进一步了解ICA对血管内皮细胞的作用,并为ICA未来的血管生成应用提供理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/47109fa97cf2/KBIE_A_2011637_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/132cb9bd38a7/KBIE_A_2011637_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/ad72b5ad72bf/KBIE_A_2011637_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/ba8d2d60fcf6/KBIE_A_2011637_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/811554b1b8c2/KBIE_A_2011637_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/cbabc9982e00/KBIE_A_2011637_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/248d08981e3b/KBIE_A_2011637_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/4eb76a879ba3/KBIE_A_2011637_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/47109fa97cf2/KBIE_A_2011637_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/132cb9bd38a7/KBIE_A_2011637_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/ad72b5ad72bf/KBIE_A_2011637_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/ba8d2d60fcf6/KBIE_A_2011637_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/811554b1b8c2/KBIE_A_2011637_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/cbabc9982e00/KBIE_A_2011637_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/248d08981e3b/KBIE_A_2011637_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/4eb76a879ba3/KBIE_A_2011637_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f84/8805869/47109fa97cf2/KBIE_A_2011637_F0008_OC.jpg

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