• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Endothelium: Journal of endothelial cell research >Effect of NADPH oxidase inhibition on E-selectin expression induced by concomitant anoxia/reoxygenation and TNF-alpha.
【24h】

Effect of NADPH oxidase inhibition on E-selectin expression induced by concomitant anoxia/reoxygenation and TNF-alpha.

机译：NADPH氧化酶抑制对缺氧/复氧和TNF-α诱导的E-选择素表达的影响。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The aim of this study was to quantify the expression of E-selectin, intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vascular endothelial cells (HUVECs) exposed to anoxia/reoxygenation (A/R) in the presence or absence of an inflammatory context (0.1 IU/ml tumor necrosis factor-alpha [TNF-alpha]) and to investigate the effects of two different NADPH inhibitors, apocynin and diphenyleneiodonium (DPI), on the expression of the endothelial cell adhesion molecules. Confluent HUVECs were exposed to anoxia for 3 hours (100% N2), followed by a reoxygenation period of 4 hours. TNF-alpha at 0.1 IU/ml was added to the medium either under normoxic conditions for 7 hours (TNF-alpha) or just before the start of anoxia (A/R + TNF-alpha). Levels of E-selectin, VCAM-1, and ICAM-1 were quantified using specific monoclonal antibodies revealed by an alkaline phosphatase-labeled goat F(ab)'2 fragment against mouse IgG antibody and the fluorescent substrate Attophos. Adhesion experiments were also performed using calcein-labeled U937 leukocytes. HUVECs submitted to A/R overexpressed E-selectin but not VCAM-1 or ICAM-1, whereas TNF-alpha at 0.1 IU/ ml increased the expression of all three adhesion molecules. In endothelial cells subjected to A/R in the presence of TNF-alpha, a synergistic increase of E-selectin expression and a synergistic adhesion of U937 cells was noted. The NADPH oxidase inhibitors apocynin and DPI both decreased significantly the U937 adhesion and the E-selectin overexpression on HUVECs submitted to A/R, TNF-alpha, or A/R + TNF-alpha. These results suggest that E-selectin expression is implicated in the leukocyte adhesion to HUVECs caused by A/R in the presence or absence of an inflammatory context. NADPH oxidase appears to participate in the E-selectin overexpression on HUVECs subjected either to A/R and/or TNF-alpha, suggesting a major role of this enzyme in the ischemia/reperfusion syndrome.
机译：这项研究的目的是量化暴露于人脐带血管内皮细胞（HUVEC）中的E-选择素，细胞间细胞粘附分子1（ICAM-1）和血管细胞粘附分子1（VCAM-1）的表达。在存在或不存在炎性环境（0.1 IU / ml肿瘤坏死因子-α[TNF-α]）的情况下进行缺氧/复氧（A / R），并研究两种不同的NADPH抑制剂，载脂蛋白和二苯并碘鎓（DPI）的作用，关于内皮细胞粘附分子的表达。将汇合的HUVEC暴露于缺氧环境3小时（100％N2），然后再充氧4小时。在常氧条件下7个小时（TNF-alpha）或刚好在缺氧开始之前（A / R + TNF-alpha），将0.1 IU / ml的TNF-α加入培养基中。 E-选择素，VCAM-1和ICAM-1的水平使用针对小鼠IgG抗体的碱性磷酸酶标记的山羊F（ab）'2片段和荧光底物Attophos揭示的特异性单克隆抗体进行定量。还使用钙黄绿素标记的U937白细胞进行粘附实验。接受A / R过表达的E-选择素但不表达VCAM-1或ICAM-1的HUVECs，而0.1 IU / ml的TNF-α则增加了所有三个粘附分子的表达。在存在TNF-α的A / R的内皮细胞中，注意到E-选择蛋白表达的协同增加和U937细胞的协同粘附。 NADPH氧化酶抑制剂Apocynin和DPI均显着降低了U937粘附和HUVEC上E-选择素过表达，使其呈A / R，TNF-α或A / R +TNF-α状态。这些结果表明，在存在或不存在炎性环境的情况下，E-选择蛋白表达与由A / R引起的白细胞对HUVEC的粘附有关。 NADPH氧化酶似乎参与了接受A / R和/或TNF-α的HUVEC的E-选择素过表达，表明该酶在缺血/再灌注综合征中起主要作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号