壳聚糖抑制高糖诱导的脂质过氧化及血管内皮细胞与单核细胞黏附

目的研究壳聚糖(chitosan)对高糖诱导细胞产生脂质过氧化及血管内皮细胞与单核细胞黏附的抑制作用。方法建立人脐静脉血管内皮细胞(HUVEC)高糖培养模型,实验分空白对照组、高糖模型组、高糖+壳聚糖组,测定细胞产生羟自由基(OH.)及脂质过氧化产物丙二醛(MDA)量;同时取单核巨噬细胞系Raw264.7,以荧光染料Rhodamin123孵育后加入以上各组,荧光摄像及比色检测单核细胞黏附数量;RT-PCR法检测血管细胞黏附分子(VCAM-1)mRNA变化。结果与空白对照组比较,高糖引起HUVEC产生OH.及MDA含量增加,黏附于HUVEC的Raw264.7数量以及VCAM-1表达升高;壳聚糖可呈浓度依赖性地抑制上述现象,但对细胞存活无明显影响。结论壳聚糖可能通过减轻自由基与脂质过氧化损伤,下调血管内皮细胞VCAM-1的表达,从而抑制高糖诱导的单核细胞与内皮细胞黏附。     

血管平滑肌细胞粘附分子的表达与心血管疾病的关系

粘附分子是指由细胞合成、存在于细胞膜或细胞外,介导细胞间、细胞与细胞基质粘附的一大类分子.与心血管疾病有关的粘附分子包括整合素家族、免疫球蛋白超家族和选择素家族.免疫球蛋白超家族成员细胞间粘附分子(intercellular adhesion molecule-1,ICAM-1)和血管细胞粘附分子(vascular cell adhesion molecule-1,VCAM-1)在白细胞向激活的内皮细胞粘附过程中起重要作用.血管内皮细胞表达粘附分子的作用已比较清楚,但几年前有人发现在动脉粥样硬化血管壁的内膜平滑肌细胞也表达ICAM-1和VCAM-1,这就引起了与这些分子相关问题的探讨.本文就ICAM-1和VCAM-1在血管平滑肌细胞表达的调节及在动脉粥样硬化(AS)和血管再狭窄发生、发展中的作用作一综述.     

染料木素对脂多糖诱导的人单核细胞与主动脉内皮细胞黏附的影响

目的 探讨染料木素对脂多糖(LPS)同时诱导的人单核细胞(THP-1)与人主动脉内皮细胞(HAEC)黏附的影响作用.方法 分别培养THP-1细胞与HAEC细胞,用不同浓度染料木素预处理两种细胞30 min,然后用LPS同时诱导两种细胞4h,将THP-1细胞加入到HAEC细胞中共培养1h,用孟加拉玫瑰红法检测THP-1细胞与HAEC细胞黏附情况;用酶联免疫吸附法检测细胞培养液上清中血管细胞黏附分子-1(VCAM-1)、细胞间黏附分子-1(ICAM-1)的浓度.结果 LPS能促使THP-1细胞与HAEC细胞黏附,促进VCAM-1和ICAM-1释放;加入染料木素后,两种细胞的黏附量及VCAM-1和ICAM-1的释放呈浓度依赖性减少(P＜0.05).结论 染料木素对脂多糖同时诱导的THP-1细胞与HAEC细胞的黏附有抑制作用.     

美沙拉嗪口服联合灌肠对溃疡性结肠炎患者的疗效及ICAM-1、VCAM-1的影响

目的 探讨美沙拉嗪口服联合灌肠对溃疡性结肠炎患者的疗效及细胞间黏附分子-1(intercellular cell adhesion molecule-1,ICAM-1)、血管细胞黏附分子(Vascular cell adhesion molecule-1,VCAM-1)的影响.方法 将2019年6月～2021年6月收治...     

盐酸埃他卡林对同型半胱氨酸致内皮细胞损伤的保护作用研究

高浓度同型半胱氨酸具有血管内皮细胞毒性。高血压病理过程中存在血管内皮细胞功能紊乱。盐酸埃他卡林（Iptakalim hydrochloride，Ipt）为新型降血压药物。本实验以逆转录-聚合酶链式反应检测单核细胞趋化蛋白-1（monocyte chemoattractant protein-1，MCP-1）、细胞间粘附分子-1（intercellular adhesive molecule-1，ICAM-1）、血管细胞黏附分子-1（vascular cell adhesive moleculel-1，VCAM-1）mRNA表达水平，观察埃他卡林对同型半胱氨酸（homocysteine，HCY）诱导内皮细胞损伤的作用。     

脂联素对大鼠血管平滑肌细胞VCAM-1和ICAM-1表达的影响

目的 探讨脂联素对肿瘤坏死因子α(TNF-α)诱导大鼠主动脉血管平滑肌细胞血管细胞黏附分子1(VCAM-1)和细胞间黏附分子1(ICAM-1)的表达及其意义.方法 复苏培养大鼠血管平滑肌细胞,通过逆转录聚合酶链式反应(RT-PCR)和免疫蛋白印迹法(Western blot)观察脂联素对TNF-α诱导的血管平滑肌细胞VCAM-1、ICAM-1蛋白及mRNA的影响.结果 TNF-α(10 ng/ml)刺激后血管平滑肌细胞VCAM-1和ICAM-1表达明显增强(P<0.01);脂联素对其则呈浓度依赖性抑制作用.结论 脂联素可抑制TNF-α诱导的血管平滑肌细胞VCAM-1和ICAM-1的表达,这可能对减轻血管壁的炎症反应、延缓动脉粥样硬化的发生、发展起一定作用.     

血管平滑肌细胞粘附分子的表达与心血管疾病的关系

粘附分子是指由细胞合成、存在于细胞膜或细胞外,介导细胞间、细胞与细胞基质粘附的一大类分子。与心血管疾病有关的粘附分子包括整合素家族、免疫球蛋白超家族和选择素家族。免疫球蛋白超家族成员细胞间粘附分子（intercellular adhesion molecule-1,ICAM-1）和血管细胞粘附分子（vascular cell adhesionmolecule-1,VCAM-1）在白细胞向激活的内皮细胞粘附过程中起重要作用。血管内皮细胞表达粘附分子的作用已比较清楚,但几年前有人发现在动脉粥样硬化血管壁的内膜平滑肌细胞也表达ICAM-1和VCAM-1,这就引起了与这些分子相关问题的探讨。本文就ICAM-1和VCAM-1在血管平滑肌细胞表达的调节及在动脉     

氢气促进人脐静脉内皮细胞增殖和抑制黏附分子释放的机制研究

目的 探究氢气对脂多糖诱导的人脐静脉内皮细胞(HUVEC)中miR-126及其潜在靶点细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)和E-选择素(E-selectin)表达的影响。方法 分4组培养HUVEC,采用不同浓度(0、0.01、0.1、1.0μg·mL^-1)的脂多糖处理24 h;确定100 ng·mL^-1为最佳诱导浓度，建立动脉粥样硬化炎症细胞模型，将细胞分为正常组、模型组、模型+氢气组、模型+阿托伐他汀组；采用CCK-8法检测细胞的存活率，RT-qPCR检测miR-126和黏附分子ICAM-1、VCAM-1、E-selectin在HUVEC中的表达。结果 采用100 ng·mL^-1脂多糖可成功诱导动脉粥样硬化炎症细胞模型；与模型组比较，氢气可显著促进细胞增殖，上调miR-126的表达，下调ICAM-1、VCAM-1、E-selectin的表达，效果与阿托伐他汀相近。结论 氢气可能通过上调miR-126的表达来发挥促进HUVEC增殖和抑制黏附分子释放的作用。     

ICAM-1、VCAM-1在脑缺血损伤炎症机制中的作用及调控

细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)在脑缺血损伤炎症过程中起着重要作用。脑缺血后ICAM-1和VCAM-1表达增加;ICAM-1、VCAM-1介导循环中的白细胞与内皮细胞黏附,进而浸润到血管外脑实质,导致缺血后炎症;抑制ICAM-1、VCAM-1表达及作用可减轻脑缺血损伤。     

血管细胞黏附分子-1与脑缺血再灌注损伤研究进展

近年来,黏附分子在脑缺血再灌注损伤中的作用已成为研究的热点之一[1].血管细胞黏附分子-1(vascular cell adhesion molecule-1,VCAM-1)是一种重要的黏附分子,现就其与脑缺血再灌注损伤的关系做一综述.     

丙丁酚抑制体外氧化低密度脂蛋白诱导的单核细胞对内皮细胞的粘附

目的:研究丙丁酚抑制体外氧化低密度脂蛋白诱导的单核细胞对内皮细胞的粘附机制.方法:采用酶联免疫法检测丙丁酚对内皮细胞粘附分子、细胞间粘附分子1(ICAM-1)、血管细胞粘附分子1 (VCAM-1)、P-选择素和E-选择素表达的影响,对比分析丙丁酚和上述粘附分子单克隆抗体抑制氧化低密度脂蛋白诱导的单核细胞对内皮细胞的粘附作用.结果:丙丁酚呈浓度依赖性抑制氧化低密度脂蛋白诱导的单核细胞对内皮细胞的粘附,丙丁酚浓度从10μmol/L增加到80μmol/L,单核细胞对内皮细胞的粘附从16.7％降低至7.0％(P<0.01),同时ICAM-1和P-选择素表达分别被抑制75％和72％(P相似文献   

Manassantin a and b isolated fromSaururus chinensis inhibit TNF-α-induced Cell adhesion molecule expression of human umbilical vein endothelial cells

Leukocyte adhesion to the vascular endothelium is a critical initiating step in inflammation and atherosclerosis. We have herein studied the effect of manassantin A (1) and B (2), dineolignans, on interaction of THP-1 monocytic cells and human umbilical vein endothelial cells (HUVEC) and expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in HUVEC. When HUVEC were pretreated with 1 and 2 followed by stimulation with TNF-alpha, adhesion of THP-1 cells to HUVEC decreased in dose-dependent manner with IC50 values of 5 ng/mL and 7 ng/mL, respectively, without cytotoxicity. Also, 1 and 2 inhibited TNF-alpha-induced up-regulation of ICAM-1, VCAM-1 and E-selectin. The present findings suggest that 1 and 2 prevent monocyte adhesion to HUVEC through the inhibition of ICAM-1, VCAM-1 and E-selectin expression stimulated by TNF-alpha, and may imply their usefulness for the prevention of atherosclerosis relevant to endothelial activation.     

Inhibitory activity of stilbenes from medicinal plants on the expression of cell adhesion molecules on THP1 cells

The inhibitory activity of stilbenes isolated from medicinal plants on cell adhesion molecules on the surface of THP-1 human monocytic cell lines was investigated. Among ten stilbenes tested, four stilbenes displayed a significant inhibitory activity on the expression of both intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). A cell-to-cell adhesion assay showed that 3,5-dihydroxy-4'-methoxystilbene and 2,3,4',5-tetrahydroxystilbene-2-O-beta-D-glucopyranoside as well as resveratrol blocked significantly TNF-alpha-inducing cell-cell adhesion between human umbilical vein endothelial cells (HUVEC) and THP-1 cells.     

Cariporide对LPC诱导单核细胞与内皮细胞粘附及粘附分子表达的抑制作用

目的研究Cariporide对溶血性磷脂酰胆碱(LPC)诱导的单核细胞与血管内皮细胞粘附以及细胞间粘附分子(ICAM-1)、P-选择素(P-selectin)表达的影响。方法人外周血液单核细胞采用Ficoll-Hypaque分离方法获得。在培养的小牛胸主动脉内皮细胞模型上,用蛋白质定量分析方法测定单核细胞与内皮细胞的粘附率;用酶联免疫吸附分析(ELISA)检测P-selectin和ICAM-1在内皮细胞的表达水平;用BCECF荧光染料测量细胞内pH值。结果LPC5mg·L-1明显促进单核细胞与内皮细胞粘附。Cariporide5、10和20μmol·L-1剂量依赖性地抑制LPC诱导的单核细胞与内皮细胞粘附及粘附分子表达,使粘附率从36%分别降至23%、18%和16%,使LPC诱导的P-selectin、ICAM-1在内皮细胞上表达率分别从170%降到142%、122%和121%以及从327%分别降至208%、148%和134%。Cariporide降低了内皮细胞内pH值。结论Cariporide对LPC诱导的单核细胞与内皮细胞的粘附以及P-selectin、ICAM-1的表达有明显抑制作用。其作用机制可能与Cariporide抑制Na+/H+交换蛋白、降低细胞内pH值有关。     

Nafamostat Mesilate Inhibits TNF-α-Induced Vascular Endothelial Cell Dysfunction by Inhibiting Reactive Oxygen Species Production

Nafamostat mesilate (NM) is a serine protease inhibitor with anticoagulant and anti-inflammatory effects. NM has been used in Asia for anticoagulation during extracorporeal circulation in patients undergoing continuous renal replacement therapy and extra corporeal membrane oxygenation. Oxidative stress is an independent risk factor for atherosclerotic vascular disease and is associated with vascular endothelial function. We investigated whether NM could inhibit endothelial dysfunction induced by tumor necrosis factor-α (TNF-α). Human umbilical vein endothelial cells (HUVECs) were treated with TNF-α for 24 h. The effects of NM on monocyte adhesion, vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) protein expression, p38 mitogen-activated protein kinase (MAPK) activation, and intracellular superoxide production were then examined. NM (0.01~100 µg/mL) did not affect HUVEC viability; however, it inhibited the increases in reactive oxygen species (ROS) production and p66shc expression elicited by TNF-α (3 ng/mL), and it dose dependently prevented the TNF-α-induced upregulation of endothelial VCAM-1 and ICAM-1. In addition, it mitigated TNF-α-induced p38 MAPK phosphorylation and the adhesion of U937 monocytes. These data suggest that NM mitigates TNF-α-induced monocyte adhesion and the expression of endothelial cell adhesion molecules, and that the anti-adhesive effect of NM is mediated through the inhibition of p66shc, ROS production, and p38 MAPK activation.     

Inhibitory effect of reinioside C on monocyte–endothelial cell adhesion induced by oxidized low-density lipoprotein via inhibiting NADPH oxidase/ROS/NF-κB pathway

Monocyte adhesion to activated vascular endothelial cells is the critical event in the initiation of atherosclerosis. Adhesion molecules are inflammatory markers, which are upregulated by oxidized low-density lipoprotein (ox-LDL) and play a pivotal role in atherogenesis. In present study, the effect of reinioside C, a major compound of Polygala fallax Hemsl., on adhesion of monocytes to endothelial cells induced by ox-LDL was investigated. The results showed that incubation of endothelial cells with ox-LDL (100?µg/mL) for 24 h markedly increased the expression of ICAM-1 and P-selectin and enhanced the adhesion of monocytes to endothelial cells. Pretreatment with reinioside C (1, 3, or 10?µM) dose-dependently decreased ox-LDL-induced upregulation of expression of ICAM-1 and P-selectin and the enhanced adhesion of monocytes to endothelial cells. To determine the role of NADPH oxidase/reactive oxygen species (ROS)/nuclear factor-κB (NF-κB) pathway, endothelial cells were treated with ox-LDL (100?µg/mL) for 2 h, and NADPH oxidase subunit (Nox 2 and p22^phox) mRNA expression, intracellular ROS level, and NF-κB activity were measured. The results showed that reinioside C attenuated ox-LDL-induced NADPH oxidase subunit (Nox 2 and p22^phox) mRNA expression, generation of ROS, and activation of NF-κB in endothelial cells in a dose-dependent manner; the two latter effects were inhibited by pyrollidine dithiocarbamate, the inhibitor of NF-κB. These findings suggest that reinioside C attenuates ox-LDL-induced expression of adhesion molecules (P-selectin and ICAM-1) and the adhesion of monocytes to endothelial cells by inhibiting NADPH oxidase/ROS/NF-κB pathway.     

Anti-atherosclerotic Activity of Platycodin D Derived from Roots of <i>Platycodon grandiflorum</i> in Human Endothelial Cells

This study examined the effects of platycodin D (PD), a triterpene saponin from the the root of Platycodon grandiflorum A.DC on human umbilical vein endothelial cells (HUVECs) in vitro, which were pre-treated with PD (0.01, 0.15, 0.25?mg/mL), respectively, and treated with 50?mg/L oxidized low-density lipoprotein (oxLDL). The levels of nitric oxide (NO) and malonaldehyde (MAD) in the culture medium, vascular cell adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1) mRNA expression in endothelium cells and the adhesion of monocytes to endothelial cells were measured. The results showed that PD increased NO concentration and decreased MDA level induced by oxLDL in the medium of endothelial cells. Moreover, PD significantly inhibited the oxLDL-induced increase in monocyte adhesion to endothelial cells as well as decreasing mRNA expression levels of VCAM-1 and ICAM-1 on these cells. Based on these results, it is suggested that PD is a promising anti-atherosclerotic activity, which is at least in part the result of its increasing NO concentration, reducing the oxLDL-induced cell adhesion molecule expression in endothelial cells and the endothelial adhesion to monocytes.