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阿斯帕拉酮可预防血管内皮生长因子诱导的人主动脉内皮细胞脂质过氧化、迁移、管腔形成及功能障碍。

Aspalatone Prevents VEGF-Induced Lipid Peroxidation, Migration, Tube Formation, and Dysfunction of Human Aortic Endothelial Cells.

作者信息

Sonowal Himangshu, Pal Pabitra B, Shukla Kirtikar, Ramana Kota V

机构信息

Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA.

出版信息

Oxid Med Cell Longev. 2017;2017:2769347. doi: 10.1155/2017/2769347. Epub 2017 Jan 24.

DOI:10.1155/2017/2769347
PMID:28243353
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5294669/
Abstract

Although aspalatone (acetylsalicylic acid maltol ester) is recognized as an antithrombotic agent with antioxidative and antiplatelet potential; its efficacy in preventing endothelial dysfunction is not known. In this study, we examined the antiangiogenic, antioxidative, and anti-inflammatory effect of aspalatone in human aortic endothelial cells (HAECs). Specifically, the effect of aspalatone on VEGF-induced HAECs growth, migration, tube formation, and levels of lipid peroxidation-derived malondialdehyde (MDA) was examined. Our results indicate that the treatment of HAECs with aspalatone decreased VEGF-induced cell migration, tube formation, and levels of MDA. Aspalatone also inhibited VEGF-induced decrease in the expression of eNOS and increase in the expression of iNOS, ICAM-1, and VCAM-1. Aspalatone also prevented the VEGF-induced adhesion of monocytes to endothelial cells. Furthermore, aspalatone also prevented VEGF-induced release of inflammatory markers such as Angiopoietin-2, Leptin, EGF, G-CSF, HB-EGF, and HGF in HAECs. Thus, our results suggest that aspalatone could be used to prevent endothelial dysfunction, an important process in the pathophysiology of cardiovascular diseases.

摘要

尽管阿沙帕洛酮(乙酰水杨酸麦芽酚酯)被认为是一种具有抗氧化和抗血小板潜力的抗血栓形成剂,但其在预防内皮功能障碍方面的功效尚不清楚。在本研究中,我们检测了阿沙帕洛酮在人主动脉内皮细胞(HAECs)中的抗血管生成、抗氧化和抗炎作用。具体而言,检测了阿沙帕洛酮对VEGF诱导的HAECs生长、迁移、管腔形成以及脂质过氧化衍生的丙二醛(MDA)水平的影响。我们的结果表明,用阿沙帕洛酮处理HAECs可降低VEGF诱导的细胞迁移、管腔形成以及MDA水平。阿沙帕洛酮还抑制VEGF诱导的eNOS表达降低以及iNOS、ICAM-1和VCAM-1表达增加。阿沙帕洛酮还可防止VEGF诱导的单核细胞与内皮细胞的黏附。此外,阿沙帕洛酮还可防止VEGF诱导的HAECs中炎性标志物如血管生成素-2、瘦素、表皮生长因子、粒细胞集落刺激因子、肝素结合表皮生长因子和肝细胞生长因子的释放。因此,我们的结果表明,阿沙帕洛酮可用于预防内皮功能障碍,这是心血管疾病病理生理学中的一个重要过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/c11721a63fe3/OMCL2017-2769347.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/8343017ba95f/OMCL2017-2769347.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/82dd68780528/OMCL2017-2769347.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/781d734f25d7/OMCL2017-2769347.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/e764699f7fd3/OMCL2017-2769347.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/a3d39f870b1f/OMCL2017-2769347.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/d292a7932030/OMCL2017-2769347.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/c11721a63fe3/OMCL2017-2769347.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/8343017ba95f/OMCL2017-2769347.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/82dd68780528/OMCL2017-2769347.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/781d734f25d7/OMCL2017-2769347.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/e764699f7fd3/OMCL2017-2769347.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/a3d39f870b1f/OMCL2017-2769347.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/d292a7932030/OMCL2017-2769347.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e190/5294669/c11721a63fe3/OMCL2017-2769347.007.jpg

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