砷剂治疗急性早幼粒细胞白血病高白细胞期LFA-1,Mac-1和ICAM-1

目的 :观察三氧化二砷 (As2 O3)和维甲酸 (ATRA)治疗急性早幼粒细胞白血病 (APL )患者高白细胞发生后 ,黏附分子 L FA- 1(淋巴细胞功能相关抗原 - 1)和 Mac- 1以及细胞间黏附分子 - 1(ICAM- 1)的表达。方法 :随机分两组 ,分别选用 0 .1% As2 O310 m L / d,静脉点滴 ;ATRA 2 5 mg· m- 2 · d- 1 ,分 3次口服。分别用流式细胞仪观察两组治疗前及治疗后白细胞增高期外周血白细胞上 L FA - 1和 Mac- 1的表达及其培养上清刺激内皮细胞 ICAM- 1的表达。结果 :As2 O3组和 ATRA组治疗后高白细胞时 L FA - 1分别为 (5 1.87± 17.6 5 ) %和 (4 8.32± 16 .98) % ,Mac- 1分别为 (4 5 .2 5± 19.12 ) %和 (4 3.4 5± 2 0 .6 5 ) % ,明显高于治疗前 ,两组间无明显差别。As2 O3组和 ATRA组高白细胞期 APL骨髓上清刺激内皮细胞表达 ICAM- 1增加分别为 (6 9.39± 18.4 6 ) %和 (6 4 .5 7± 7.2 4 ) % ,明显高于治疗前 (4 2 .35± 9.36 ) %和 (4 5 .5 6± 6 .86 ) %。结论 :As2 O3和 ATRA治疗 APL高白细胞的发生与诱导分化治疗过程中 APL细胞的黏附分子 L FA- 1和 Mac- 1表达增加 ,并刺激内皮细胞 ICAM- 1的增加有关 ,L FA - 1,Mac- 1和ICAM- 1互相作用 ,使 APL细胞与内皮细胞黏附增加 ,并释放入外周血增加。     

The effects of heparin on the adhesion of human peripheral blood mononuclear cells to human stimulated umbilical vein endothelial cells

1. The effects of unfractionated heparin (UH) and a selectively O-desulphated derivative of heparin (ODSH), lacking anticoagulant activity, on the adhesion of human peripheral blood mononuclear cells (HPBMNC) to human stimulated umbilical vein endothelial cells (HUVECs), were investigated. 2. For comparison, the effects of poly-L-glutamic acid (PGA), a large polyanionic molecule without sulphate groups and two different molecular weight sulphated dextrans (DS 5 k and DS 10 k) were studied. 3. UH (50 - 1000 u ml(-1)) significantly (P<0.05) inhibited the adhesion of HPBMNC to HUVECs, stimulated with IL-1beta (100 u ml(-1)), TNF-alpha (1000 u ml(-1)) or LPS (100 microg ml(-1)), when the drugs were added together with stimuli to HUVECs and coincubated for 6 h. Such effects on adhesion occurred with limited influence on expression of relevant endothelial adhesion molecules (ICAM-1 and VCAM-1). 4. UH (100 - 1000 u ml(-1)), when added to prestimulated HUVECs, significantly (P<0.05) increased adhesion of mononuclear cells to endothelium at the higher concentrations tested, without any effect on adhesion molecule expression. In contrast, the opposite effect was observed when human polymorphonuclear leucocyte adhesion was examined, under the same experimental conditions, suggesting that the observed potentiation of HPBMNC adhesion is cell specific. 5. The effects of UH on HPBMNC adhesion were shared by the non-anticoagulant ODSH (600 - 6000 microg ml(-1)) but not by sulphated dextrans or PGA (300 - 6000 microg ml(-1)). 6. Heparin affects the adhesion of HPBMNC to stimulated endothelium, in both an inhibitory and potentiating manner, effects which are unrelated to its anticoagulant activity and not solely dependent on molecular charge characteristics.     

Peoniflorin prevents the adhesion between inflammatory endothelial cells and leukocytes through inhibiting the activation of MAPKs and NF‐κB

The vascular endothelium can be activated by multiple factors, including lipopolysaccharide (LPS) functioning as a key component of the inflammatory response. Activated endothelium promotes the recruitment of leukocytes mainly by releasing various adhesion molecules and amplifies inflammation via a feedback loop. Peoniflorin, the main active constituent of the roots of Paeonia lactiora Pall., possesses anti‐inammatory, anti‐infective, and anti‐platelet aggregative properties. To elucidate the anti‐inammatory mechanism of peoniflorin, the present study was conducted to address its effects on the adhesion of inflammatory endothelial cells to leukocytes. Peoniflorin substantially reduced adhesion of either human acute monocytic leukemia cells (THP‐1) or human acute promyelocytic leukemia cells (HL‐60) to LPS‐stimulated human umbilical vein endothelial cells (HUVECs). It also markedly down‐regulated the expression of E‐selectin at both the gene and protein levels. However, peoniflorin only slightly reduced expression of intercellular adhesion molecule‐1 (ICAM‐1). Signal pathway analysis indicated that peoniflorin reduced phosphorylation of c‐Jun NH₂‐terminal kinase (JNK) and p38 kinase, as well as the phosphorylation and degradation of IκB‐α in HUVECs. These findings suggest that prevention of the adhesion between inflammatory endothelial cells and leukocytes contributes, at least partially, to the anti‐inflammation action of peoniflorin. The anti‐adhesion mechanisms of peoniflorin were involved in the down‐regulation of the activation of mitogen‐activated protein kinases (MAPKs) and nuclear factor‐kappa B (NF‐κB), and a reduction of adhesion molecule expressions in endothelial cells. Drug Dev Res 2010.© 2010 Wiley‐Liss, Inc.     

Effects of acrolein in comparison to its prodrug cyclophosphamide on human primary endothelial cells in vitro

Cyclophosphamide (CPA) is one of the most successful anticancer prodrugs that becomes effective after biotransformation in the liver resulting in the toxic metabolite acrolein. Cancer is often accompanied by thromboembolic events, which might be a result of dysfunctional endothelial cells due to CPA treatment.Here, the effect of 1 mM CPA or acrolein (10/50/100/500 μM) on human umbilical vein endothelial cells (HUVECs) was analyzed after two days of treatment.The addition of CPA or 10 μM acrolein did not affect HUVECs. However, concentrations of 100 μM and 500 μM acrolein significantly reduced the number of adherent cells by 86 ± 13% and 99 ± 1% and cell viability by 51 ± 29% and 93 ± 8% compared to the control. Moreover, pronounced stress fibers as well as multiple nuclei were observed and von Willebrand factor (vWF) was completely released. Lactate dehydrogenase was 8.5 ± 7.0-fold and 252.9 ± 42.9-fold increased showing a loss of cell membrane integrity. The prostacyclin and thromboxane secretion was significantly increased by the addition of 500 μM acrolein (43.1 ± 17.6-fold and 246.4 ± 106.3-fold) indicating cell activation/pertubation.High doses of acrolein led to HUVEC death and loss of vWF production. This effect might be associated with the increased incidence of thromboembolic events in cancer patients treated with high doses of CPA.     

热应激诱导内皮细胞与白细胞黏附及油茶皂苷的拮抗作用

目的探讨热应激时内皮细胞与白细胞黏附的改变及油茶皂苷对此影响。方法建立人脐静脉内皮细胞(HU-VECs)热应激损伤模型,以油茶皂苷(10.0,1.0,0.1μmol.L-1)预处理细胞5 h,取培养细胞上清液测定LDH活性,HUVECs分别用于测定细胞存活率,白细胞黏附率及细胞间黏附分子-1(ICAM-1)的表达。结果热应激可引起LDH活性升高,白细胞黏附率及ICAM-1表达的增加,与对照组比较,差异具有显著性(P<0.01),但细胞存活率无明显下降。油茶皂苷呈浓度依赖性地对抗上述改变,但对细胞存活率无明显影响。结论油茶皂苷可抑制热应激诱导内皮细胞与白细胞黏附的增加,其机制可能是下调ICAM-1的表达。     

Effects of abciximab and tirofiban on vitronectin receptors in human endothelial and smooth muscle cells

human umbilical venous endothelial cells. 7E3 binding correlated with alphavbeta3-expression in all cell types. Integrin-mediated cell functions were analysed with adhesion and spreading assays on vitronectin. In human umbilical venous endothelial cells, these functions were mediated by alphavbeta3 and in human iliac arterial smooth muscle cells by alphavbeta5. In human umbilical venous smooth muscle cells, both vitronectin receptors were involved. Abciximab potently inhibited alphavbeta3-mediated cell adhesion and spreading. With tirofiban, no significant inhibition of vascular cell functions was observed. The present data demonstrate that vitronectin-cell interactions in vascular cells are mediated via two distinct integrin-receptors, alphavbeta3 and alphavbeta5. Abciximab, which solely inhibits alphavbeta3-mediated cell functions, may be particularly effective in human endothelium and in beta3-integrin expressing vascular smooth muscle cells.     

Protective effects of ligustrazine on TNF-α-induced endothelial dysfunction

To investigate the effects of Ligustrazine, a compound derived from chuanxiong, on tumor necrosis factor-α (TNF-α) stimulated endothelial cells. Human umbilical vein endothelial cells (HUVECs) were stimulated with TNF-α in vitro. Nitric oxide (NO) was measured as a standard of endothelial dysfunction. Two important indicators of autoimmunity, intracellular adhesion molecular-1 (ICAM-1) and heat shock protein 60 (HSP60), were selected to evaluate the influence of Ligustrazine on HUVECs. Ligustrazine (40 μg/ml) significantly reversed the decrease in NO production induced by TNF-α (5 ng/ml) in HUVECs. The expressions of ICAM-1 and HSP60 were increased by TNF-α treatment, but dramatically inhibited by treatment with ligustrazine in TNF-α-stimulated cells. Ligustrazine increased the production of NO in HUVECs and had an immunomodulatory effect on HUVECs stimulated with TNF-α by down-regulating the expression of ICAM-1 and HSP60. These results suggest that ligustrazine protects the endothelium via inhibition of immunological reactions, preventing atherosclerosis.     

Cytotoxicity,oxidative stress and inflammation induced by ZnO nanoparticles in endothelial cells: interaction with palmitate or lipopolysaccharide

Recent studies showed that ZnO nanoparticles (NPs) might induce the toxicity to human endothelial cells. However, little is known about the interaction between ZnO NPs and circulatory components, which is likely to occur when NPs enter the blood. In this study, we evaluated ZnO NP‐induced cytotoxicity, oxidative stress and inflammation in human umbilical vein endothelial cells (HUVECs), with the emphasis on the interaction with palmitate (PA) or lipopolysaccharide (LPS), because PA and LPS are normal components in human blood that increase in metabolic diseases. Overall, ZnO NPs induced cytotoxicity and intracellular reactive oxygen species (ROS) at a concentration of 32 μg ml⁻¹, but did not significantly affect the release of inflammatory cytokines or adhesion of THP‐1 monocytes to HUVECs. In addition, exposure to ZnO NPs dose‐dependently promoted intracellular Zn ions in HUVECs. PA and LPS have different effects. Two hundred μm PA significantly induced cytotoxicity and THP‐1 monocyte adhesion, but did not affect ROS or release of inflammatory cytokines. In contrast, 1 μg ml⁻¹ LPS significantly induced ROS, release of inflammatory cytokines and THP‐1 monocyte adhesion, but not cytotoxicity. The presence of ZnO NPs did not significantly affect the toxicity induced by PA or LPS. In addition, the accumulation of Zn ions after ZnO NP exposure was not significantly affected by the presence of PA or LPS. We concluded that there was no interaction between ZnO NPs and PA or LPS on toxicity to HUVECs in vitro . Copyright © 2016 John Wiley & Sons, Ltd.     

灵芝多糖肽对人脐静脉内皮细胞氧化损伤的保护作用

目的研究灵芝多糖肽对人脐静脉内皮细胞(HU-VECs)氧化损伤的保护作用。方法原代培养人脐静脉内皮细胞,CD31免疫荧光法鉴定细胞。以叔丁基氢过氧化物(tBOOH)为氧化剂损伤细胞,造成氧化损伤模型,培养液中加入不同浓度灵芝多糖(6.125、12.5、25、50、100mg·mL-1),以CCK-8法检测细胞存活率;Hoechst333258检测细胞氧化损伤引起的凋亡;比色法检测Caspase-3活性变化;电镜检测细胞及细胞器形态学改变。结果灵芝多糖(6.125、12.5、25、50、100mg·mL-1)可减轻叔丁基氢过氧化物对HUVECs的氧化损伤,CCK-8检测灵芝多糖给药组,HUVEC细胞存活率增加。Hoechst33258检测给药组细胞凋亡数量较损伤组减少。比色法检测损伤组Caspase-3活性明显增高,给药组较损伤组减少。电镜可见灵芝多糖给药组减轻细胞器的氧化损伤,减少细胞凋亡。结论灵芝多糖肽(GLPP)对人脐静脉内皮细胞氧化损伤具有保护作用。     

辛伐他汀抑制白细胞介素-18诱导的人脐静脉内皮细胞Fractalkine表达和黏附作用

目的观察辛伐他汀(simvastatin)对白细胞介素-18(interleukine-18,IL-18)诱导人脐静脉内皮细胞(HUVECs)上调表达Fractalkine(FKN)的影响以及对FKN黏附作用的干预效应。方法应用逆转录-聚合酶链反应(RT-PCR)检测HEUVCs FKN的表达;应用Flowchamber观察FKN介导的HUVECs与单核细胞THP-1的黏附。结果IL-18可诱导FKN mRNA表达增加,FKN表达上调可明显增加对单核细胞THP-1的黏附作用(P<0.01);PDTC能够抑制FKN表达及细胞黏附(P<0.01);辛伐他汀能够抑制FKN mRNA表达(P<0.01),100μmol·L-1辛伐他汀可抑制细胞黏附(P<0.01)。结论辛伐他汀能够抑制FKN的表达以及FKN介导的黏附作用。     

阿托伐他汀对内皮细胞微粒诱导人脐静脉内皮细胞VCAM-1和ICAM-1表达的影响

目的:探讨阿托伐他汀对内皮细胞微粒(EMPs)诱导的人脐静脉内皮细胞(HUVECs)表达血管细胞粘附分子(VCAM)-1和细胞间粘附分子(ICAM)-1的影响。方法:取生长良好的第4,5代人脐静脉内皮细胞,将细胞分为3大组:对照组、EMPs组、EMPs+阿托伐他汀组。对照组加入培养基,EMPs组以不同浓度的EMPs(0/mL,1×102/mL,1×103/mL,1×104/mL,1×105/mL)与HUVECs共同孵育24 h,EMPs+阿托伐他汀组以不同浓度的阿托伐他汀(0.05,0.1,1.0,10μmol.L-1)与HUVECs作用1 h后,加入105/mL EMPs共同孵育24 h。分别采用实时荧光定量聚合酶链反应和蛋白免疫印迹方法检测VCAM-1和ICAM-1 mRNA和蛋白的表达。结果:HUVECs受EMPs刺激后,VCAM-1和ICAM-1 mRNA及蛋白表达呈浓度依赖性增加,阿托伐他汀可不同程度上抑制EMPs的作用。结论:阿托伐他汀抗动脉粥样硬化作用可能部分与抑制EMPs诱导的内皮细胞VCAM-1和ICAM-1的表达有关。     

替米沙坦对AGEs诱导人内皮细胞表达VCAM-1及MCP-1的作用和机制

目的 通过观察替米沙坦对晚期糖基化终末产物（AGEs）诱导的人脐静脉内皮细胞表达血管细胞黏附因子-1（VCAM-1）和单核细胞趋化蛋白-1（MCP-1）的影响,研究替米沙坦对AGEs所致动脉粥样硬化（AS）的干预作用和机制。方法 采用胶原酶消化法获取人脐静脉内皮细胞,分为4组：空白对照组,牛血清白蛋白（BSA）对照组,AGEs诱导组（10^-4~10^-1mg/mL）,AGEs+替米沙坦组（1、10、100 nmol/L）。活性氧检测试剂盒检测及倒置荧光显微镜观察细胞内活性氧含量,RT-PCR检测VCAM-1、MCP-1及晚期糖基化终末产物受体（RAGE）的mRNA。结果 AGEs组人内皮细胞内活性氧荧光强度增强,替米沙坦干预后降低;AGEs呈浓度依赖性地增强人内皮细胞对VCAM-1和MCP-1基因的转录,与空白对照组相比,AGEs（10^-4mg/mL）组VCAM-1和MCP-1 mRNA表达水平显著增高（0.24±0.01 vs 0.07±0.02;0.25±0.01 vs 0.18±0.03,P<0.05）;替米沙坦呈浓度依赖性地抑制人内皮细胞对VCAM-1和MCP-1基因的转录,与AGEs诱导组相比,替米沙坦（10 nmol/L）组人内皮细胞的VCAM-1和MCP-1基因转录水平显著降低（0.23±0.01 vs 0.85±0.11;0.62±0.10 vs 1.05±0.04,P<0.05）;与AGEs诱导组相比,替米沙坦（1 nmol/L）组人内皮细胞RAGE基因表达水平显著降低（0.64±0.03 vs 1.18±0.10,P<0.05）。结论 AGEs增强人内皮细胞表达VCAM-1和MCP-1;替米沙坦可能通过抑制RAGE表达来抑制AGEs诱导的人内皮炎性损伤。     

白黎芦醇对fMLP诱导中性白细胞与人脐静脉内皮细胞粘附的抑制作用及机制

目的研究白藜芦醇(resveratrol,Res)对趋化肽N-甲酰-甲硫氨酰-亮氨酰苯丙氨酸(fMLP)诱导中性白细胞与人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)的粘附及HUVECs释放可溶性粘附分子的影响。方法观察不同浓度Res对fMLP(10μmol.L-1)刺激HU-VECs与中性白细胞粘附的影响。以ELISA法测定可溶性细胞间粘附分子,血管细胞粘附分子和E-选择素。以Fura-3和海萤萤光素诱导剂为荧光指示剂分别测定中性白细胞内[Ca2+]i水平和O2.浓度。结果Res(1~50μmol.L-1)明显抑制fMLP诱导的中性白细胞与HUVECs的粘附反应,同时,明显抑制fMLP诱导粘附分子的释放效应。Res抑制中性白细胞中O2.生成和[Ca2+]i升高,其中Res5μmol.L-1和50μmol.L-1与fMLP诱导组相比具有统计学意义(P<0.01)。结论白藜芦醇通过影响中性白细胞内O2.生成和[Ca2+]i水平,抑制中性白细胞与内皮细胞的粘附以及细胞间粘附分子表达,在阻断炎性反应的发生与发展过程中发挥着重要作用。     

血管紧张素Ⅱ对培养人脐静脉内皮细胞PAI-1 tPA蛋白表达的影响

目的研究血管紧张素Ⅱ(AngⅡ)对人脐静脉内皮细胞(HUVECs)1型纤溶酶原激活物抑制剂(PAI-1)、组织型纤溶酶原激活剂(tPA)蛋白的释放及活性的影响。方法将不同浓度的AngⅡ(1×10-9~1×10-6mmol/L)与HUVECs共同孵育24h,以及将1×10-6mol/LAngⅡ与HUVECs作用不同时间(0、4、8、12、24h)后,用细胞酶联免疫法和发色底物法分别检测细胞培养液中PAI-1、tPA的含量及活性。结果1×10-6mol/LAngⅡ作用HUVECs24h后,可使细胞分泌的PAI-1含量与对照组相比明显增高[(280±16)ng/mlvs(83±11)ng/ml,P<0.01],PAI-1活性明显增高[(10.35±1.47)U/mlvs(5.65±0.44)U/ml,P<0.01],AngⅡ虽也可刺激tPA含量增加[(102±4)ng/mlvs(70±6)ng/ml,P<0.01],但PAI-1的增量是tPA增量的6~7倍[Δ(197±21)ng/mlvsΔ(31±6)ng/ml,P<0.01],AngⅡ对tPA活性无影响[(0.97±0.05)U/mlvs(0.95±0.08)U/ml,P>0.05];1×10-9~1×10-6mol/L不同浓度的AngⅡ分别作用HUVECs24h,PAI-1含量增加、活性增加与AngⅡ呈浓度依赖性相关;1×10-6mol/LAngⅡ与HUVECs分别作用4~24h,PAI-1含量及活性增加与AngⅡ作用于HUVECs的时间呈正相关。结论AngⅡ可促使HUVECs分泌PAI-1,并使其活性增加,AngⅡ虽亦可刺激tPA分泌,但作用弱于PAI-1,且对其活性无明显影响。     

Paeonol suppresses intercellular adhesion molecule-1 expression in tumor necrosis factor-alpha-stimulated human umbilical vein endothelial cells by blocking p38, ERK and nuclear factor-kappaB signaling pathways

Paeonol (2'-hydroxy-4'-methoxyacetophenone), the main active compound of the traditionally used Chinese herb Paeonia lactiflora Pallas, has anti-inflammatory, antioxidant and cardiovascular protective activities. We studied how the levels of intercellular adhesion molecule-1 (ICAM-1), one of the key molecules in the development of atherosclerosis, might be affected by paeonol in tumor necrosis factor-alpha (TNF-alpha)-activated human umbilical vein endothelial cells (HUVECs). Paeonol concentration-dependently inhibited the production of ICAM-1; it inhibited nuclear factor-kappaB (NF-kappaB) p65 translocation into the nucleus and the phosphorylation of inhibitory factor kappaBalpha (IkappaBalpha). It also blocked the TNF-alpha-induced phosphorylation of p38 and extracellular signal-regulated kinase (ERK), which are involved in regulating ICAM-1 production by TNF-alpha. Paeonol inhibited U937 monocyte adhesion to HUVECs stimulated by TNF-alpha, suggesting that it may inhibit the binding of monocytes to endothelium by regulating the production of critical adhesion molecules by TNF-alpha. The inhibitory effect of paeonol on ICAM-1 production might be mediated by inhibiting p38, ERK and NF-kappaB signaling pathways, which are involved in TNF-alpha-induced ICAM-1 production. Thus, paeonol may be beneficial in the treatment of cardiovascular disorders such as atherosclerosis.     

Vanadium pentoxide induces activation and death of endothelial cells

Vanadium is a transition metal released into the atmosphere, as air-suspended particles, as a result of the combustion of fossil fuels and some metallurgic industry activities. Air-suspended particle pollution causes inflammation-related processes such as thrombosis and other cardiovascular events. Our aim was to evaluate the effect of vanadium pentoxide (V2O5) on endothelial cells since they are key participants in the pathogenesis of several cardiovascular and inflammatory diseases. Cell adhesion, the expression of adhesion molecules and oxidative stress, as well as proliferation, morphology and cell death of human umbilical vein endothelial cells (HUVECs) exposed to V2O5, were evaluated. Vanadium pentoxide at a 3.12 μg cm(-2) concentration induced an enhanced adhesion of the U937 macrophage cell line to HUVECs, owing to an increased expression of late adhesion molecules. HUVECs exposed to V2O5 showed an increase in ROS and nitric oxide production, and a diminished proliferation. These changes in vanadium-treated HUVECs were accompanied by severe morphological changes and apoptotic cell death. Vanadium pentoxide induced serious endothelial cell damage, probably related to the increased cardiovascular morbidity and mortality observed in individuals living in highly air-polluted areas.     

人脐静脉血管内皮细胞构建组织工程心脏瓣膜及其生理功能

目的 探讨人脐静脉血管内皮细胞(HUVECs)构建组织工程心脏瓣膜(TEHV)及其生理功能.方法 以脱细胞猪主动脉瓣作支架;将扩增的HUVECs种植在瓣膜上,体外静态构建TEHV,观察内皮细胞的形态和生长状况.收集瓣膜培养液,检测瓣膜内皮细胞分泌组织型纤溶酶原激活物(t-PA)、组织型纤溶酶原激活物抑制物(PAI-1)、前列环素(PGI2)、一氧化氮(NO)、内皮素(ET-1)的功能.结果 猪主动脉瓣膜中的细胞成分能完全去除,脱细胞瓣叶的生物力学特性同新鲜瓣叶相比无明显变化以HUVECs做种子细胞,成功构建TEHV;瓣膜表面的内皮细胞生长状态良好,长成连续的细胞层.细胞能够分泌t-PA、PAI-1、PGI2、NO、ET-1等.结论 以脱细胞猪主动脉瓣膜为支架,种植HUVECs成功构建TEHV,其表面HUVECs具有正常内皮细胞的生理功能.     

Aescin protection of human vascular endothelial cells exposed to cobalt chloride mimicked hypoxia and inflammatory stimuli

Human vascular endothelial cells (HUVECs) were exposed to CoCl2 as an in vitro model of hypoxia. Expression of VCAM-1 (vascular cell adhesion molecule), reduction of PECAM-1 (platelet endothelial cell adhesion molecule) and cytoskeletal changes without alterations in cell viability were observed. HUVECs were also exposed to Escherichia coli lipopolysaccaride (LPS) as an in vitro model of inflammation: significant IL-6 release was measured. Pre-treatment of HUVECs with aescin prevented, in a concentration-dependent fashion (0.1-1 microM), the action of CoCl2 on VCAM-1 and PECAM-1, also preserving endothelial cell morphology. Furthermore, aescin pre-treatment reduced IL-6 release from LPS-activated vascular endothelium.