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低剂量阿司匹林可促进内皮祖细胞的迁移和黏附,并防止其衰老。

Low-dose aspirin promotes endothelial progenitor cell migration and adhesion and prevents senescence.

作者信息

Hu Zhengli, Zhang Fumin, Yang Zhijian, Zhang Jinying, Zhang Dingguo, Yang Naiquan, Zhang Yuqing, Cao Kejiang

机构信息

Department of Cardiology, First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, China.

出版信息

Cell Biol Int. 2008 Jul;32(7):761-8. doi: 10.1016/j.cellbi.2008.03.004. Epub 2008 Mar 29.

Abstract

Circulating endothelial progenitor cells (EPCs) play a key role in restoring endothelial function and enhancing angiogenesis. However, the effects of low-dose aspirin on circulating EPCs are not well known. We investigated the effects of low-dose aspirin on EPC migration, adhesion, senescence, proliferation, apoptosis and endothelial nitric oxide synthase (eNOS) expression. EPC migration was detected by a modified Boyden chamber assay. EPC adhesion assay was performed by counting adherent cells on fibronectin-coated culture dishes. EPC senescence was assessed by both senescence-associated-beta-galactosidase staining and DAPI staining. EPC proliferation was analyzed by MTT assay. EPC apoptosis was evaluated by flow cytometric analysis. eNOS protein expression was measured by Western blotting analysis. Aspirin promoted EPC migratory and adhesive capacity at concentrations between 0.1 and 100micromol/L and prevented senescence at concentrations between 50 and 100micromol/L. Meanwhile, aspirin in a range of these concentrations did not affect EPC proliferation, apoptosis or eNOS expression. Our findings indicate that low-dose aspirin promotes migration and adhesion and delays the onset of senescence of EPCs.

摘要

循环内皮祖细胞(EPCs)在恢复内皮功能和促进血管生成中起关键作用。然而,低剂量阿司匹林对循环EPCs的影响尚不清楚。我们研究了低剂量阿司匹林对EPC迁移、黏附、衰老、增殖、凋亡及内皮型一氧化氮合酶(eNOS)表达的影响。通过改良的Boyden小室试验检测EPC迁移。通过计数纤连蛋白包被的培养皿上的贴壁细胞进行EPC黏附试验。通过衰老相关β-半乳糖苷酶染色和DAPI染色评估EPC衰老。通过MTT试验分析EPC增殖。通过流式细胞术分析评估EPC凋亡。通过蛋白质印迹分析测定eNOS蛋白表达。阿司匹林在0.1至100微摩尔/升的浓度范围内促进EPC迁移和黏附能力,并在50至100微摩尔/升的浓度范围内防止衰老。同时,在这些浓度范围内的阿司匹林不影响EPC增殖、凋亡或eNOS表达。我们的研究结果表明,低剂量阿司匹林促进EPC迁移和黏附,并延迟EPC衰老的发生。

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