Suppr超能文献

人内皮细胞中细胞间黏附分子1(ICAM-1)和血管细胞黏附分子1(VCAM-1)的变化

Alterations in intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in human endothelial cells.

作者信息

Habas Khaled, Shang Lijun

机构信息

School of Chemistry and Biosciences, Faculty of Life Sciences, University of Bradford, Bradford, Richmond Road, West Yorkshire, BD7 1DP, UK.

School of Chemistry and Biosciences, Faculty of Life Sciences, University of Bradford, Bradford, Richmond Road, West Yorkshire, BD7 1DP, UK.

出版信息

Tissue Cell. 2018 Oct;54:139-143. doi: 10.1016/j.tice.2018.09.002. Epub 2018 Sep 12.

Abstract

Alterations of Endothelial cells (ECs) play a critical role in different pathogenesis of many serious human diseases, and dysfunction of the vascular endothelium is an indicator for human disorders. Endothelial dysfunction is considered to be an early indicator for atherosclerosis, which is characterised by overexpression of adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Hydrogen peroxide (HO) released via neutrophils is an important mediator of endothelial cell function. Ambient production of superoxide anion (O) and subsequently HO at low levels is critical for regulating endothelial cell functions and proliferation. In this study, we investigated the effects of HO on the expression of adhesion molecules VCAM-1 and ICAM-1 in cultured human umbilical vein endothelial cells (HUVECs). Intracellular superoxide anion production was detected by using p-Nitro Blue Tetrazolium (NBT) assay. Our results showed that administration of 100μM of HO on HUVECs for 2, 6, 12 and 24 h induced a time-dependent increase in ICAM-1 and VCAM-1 mRNA and protein expression levels with a significant increase observed from 6 h. HUVECs exposed to HO exhibit increased O, suggesting that HO induced oxidative stress may be a reasonable for atherosclerosis. This increase can be reduced by the flavonoid, N-acetyl cysteine (NAC). The modulation of endothelial cell function through this mechanism may underlie the contribution of HO to the development of vascular disease.

摘要

内皮细胞的改变在许多严重人类疾病的不同发病机制中起着关键作用,而血管内皮功能障碍是人类疾病的一个指标。内皮功能障碍被认为是动脉粥样硬化的早期指标,其特征是包括细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)在内的黏附分子过度表达。通过中性粒细胞释放的过氧化氢(H₂O₂)是内皮细胞功能的重要介质。超氧阴离子(O₂⁻)的环境产生以及随后低水平的H₂O₂对于调节内皮细胞功能和增殖至关重要。在本研究中,我们研究了H₂O₂对培养的人脐静脉内皮细胞(HUVECs)中黏附分子VCAM-1和ICAM-1表达的影响。使用对硝基蓝四唑(NBT)测定法检测细胞内超氧阴离子的产生。我们的结果表明,用100μM的H₂O₂处理HUVECs 2、6、12和24小时会导致ICAM-1和VCAM-1 mRNA及蛋白表达水平呈时间依赖性增加,从6小时起观察到显著增加。暴露于H₂O₂的HUVECs表现出O₂⁻增加,这表明H₂O₂诱导的氧化应激可能是动脉粥样硬化的一个合理原因。这种增加可以被类黄酮N-乙酰半胱氨酸(NAC)降低。通过这种机制对内皮细胞功能的调节可能是H₂O₂对血管疾病发展起作用的基础。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验