血小板微颗粒对人脐静脉内皮细胞黏附因子表达的影响

目的:探讨血小板微颗粒(PMPs)对人脐静脉内皮细胞黏附因子表达的影响及PMPs在冠心病中的可能作用机制。方法:分离制备血小板微颗粒,与人脐静脉内皮细胞CRL-1730共培养,应用半定量逆转录聚合酶链反应技术测定不同浓度PMPs作用不同时间的内皮细胞黏附因子E-选择素、细胞间黏附分子(ICAM)-1、血管细胞间黏附分子(VCAM)-1的表达。结果:当PMPs达到一定浓度,可促使内皮细胞(CRL-1730)表达E-选择素、ICAM-1和VCAM-1升高,差异有统计学意义(P<0.05);而PMPs刺激内皮细胞(CRL-1730)不同时间,E-选择素、ICAM-1的表达差异无统计学意义(均P>0.05)。结论:PMPs可促使体外培养的人脐静脉内皮细胞(CRL-1730)表达E-选择素、ICAM-1和VCAM-1升高,从一方面解释了PMPs在冠心病中的可能的作用机制。     

血小板微颗粒对人脐静脉内皮细胞粘附因子表达的影响

目的：探讨血小板微颗粒对人脐静脉内皮细胞粘附因子E-selectin、ICAM-1、VCAM-1表达的影响,以揭示血小板微颗粒在冠心病中的可能作用机制。方法：分离制备血小板微颗粒,与人脐静脉内皮细胞CRL-1730共培养,应用半定量逆转录聚合酶链反应技术测定不同浓度血小板微颗粒作用不同时间,内皮细胞粘附因子E-selectin、ICAM-1、VCAM-1的表达。结果:当PMPS达到一定浓度,可促使内皮细胞(CRL-1730)表达E-selectin、ICAM-1和VCAM-1升高,差异有统计学意义（p<0.05）;而PMPs刺激内皮细胞(CRL-1730)不同时间,E-selectin、ICAM-1的表达无差异（p>0.05）。结论: PMPs可促使体外培养的人脐静脉内皮细胞(CRL-1730)表达E-selectin、ICAM-1和VCAM-1升高,从而从一方面解释了PMPs在冠心病中的可能的作用机制。     

小干扰RNA沉默p65基因对人脐静脉内皮细胞再灌注后促炎因子表达的影响

目的 通过小干扰RNA (siRNA) 研究沉默p65对人脐静脉内皮细胞（HUVECs）再灌注损伤后促炎因子表达水平的影响。方法 分为4组对HUVECs进行培养，即正常培养+siRNA阴性对照转染组、缺血再灌注+siRNA阴性对照转染组、正常培养+p65 siRNA转染组和缺血再灌注+p65 siRNA转染组。模拟缺血再灌注通过在模拟缺血培养液中培养HUVECs 30分钟后换正常培养液再培养4小时而实现，siRNA转染则在模拟缺血再灌注培养前48小时对HUVECs转染p65 siRNA或阴性对照siRNA。实时定量PCR和酶联免疫吸附法分别检测p65 siRNA对TNF-α、ICAM-1 mRNA和蛋白表达水平的影响。 结果 模拟缺血再灌注刺激TNF-α、ICAM-1的mRNA和蛋白表达水平显著升高( P < 0.05) 。p65 siRNA转染显著抑制模拟缺血再灌注所诱导的HUVECs的TNF-α、ICAM-1 的mRNA和蛋白表达水平( P < 0.05)。结论 p65 siRNA通过沉默p65，抑制模拟缺血再灌注诱导的TNF-α和ICAM-1表达水平。     

血管内皮细胞体外损伤模型

目的 研究系统性红斑狼疮(SLE)患者血管内皮细胞(VEC)体外损伤模型的建立方法,为进一步治疗SLE血管病变的研究奠定基础.方法 收集5例活动期SLE患者血清,以此血清刺激人脐静脉内皮细胞株(ECV-304),酶联免疫吸附法(ELISA)检测培养上清液中血管假性血友病因子(vWF)、可溶性血栓调节蛋白(sTM)含量.结果 SLE患者血清致ECV-304培养上清液中vWF、sTM含量增加,与对照组比较(P<0.05).结论 活动期SLE患者血清体外可损伤血管内皮细胞.     

乙醇诱导人脐静脉内皮细胞凋亡及对ICAM-1蛋白表达影响的研究

目的:研究乙醇体外诱导人脐静脉内皮细胞(HUVEC)凋亡,及对细胞间黏附分子(ICAM-1)蛋白表达的影响。方法:以不同浓度乙醇(50、100和200mmol/L)作用于体外培养的人脐静脉内皮细胞24h,四甲基偶氮唑盐(MTT)比色法测定各组细胞活力;流式细胞仪检测细胞凋亡率;酶联免疫吸附法检测ICAM-1蛋白表达。结果:乙醇能抑制内皮细胞活力,促进细胞凋亡,增加ICAM-1表达,并呈浓度依赖性。结论:乙醇能诱导内皮细胞损伤,其机制可能与促进细胞凋亡、影响ICAM-1蛋白表达有关。     

门脉高压患者血浆刺激血管内皮细胞Hsp90表达的试验研究

目的:研究肝硬化门静脉高压症患者血浆对血管内皮细胞热休克蛋白(Hsp90)表达的影响,以了解Hsp90在肝硬化门脉高压形成中的作用。方法:应用免疫组织化学染色法检测Hsp90在正常人血浆和肝硬化门静脉高压症患者血浆刺激人脐静脉血管内皮细胞(HUVEC)中的表达情况。结果:通过组织化学染色图像定量分析显示肝硬化患者血浆处理的HUVEC表达的Hsp90平均灰度值为1.925,正常人血浆处理为1.416,经统计学分析肝硬化患者血浆处理HUVEC表达的Hsp90高于正常人血浆处理组(P<0.05)。结论:肝硬化门脉高压血浆可以刺激血管内皮细胞使Hsp90表达增加,Hsp90可能促进肝硬化门脉高压的形成。     

同型半胱氨酸对人脐静脉内皮细胞MCP-1 mRNA表达的影响

目的:探讨同型半胱氨酸(Hcy)对人脐静脉内皮细胞单核细胞趋化蛋白-1(MCP-1)mRNA表达的影响.方法:人脐静脉内皮细胞CRL-1730融合至90%分别加入不同浓度Hcy:空白组0 mmol/L、生理剂量组0.01 mmol/L、病理剂量组0.1 mmol/L、非毒性药理剂量组1.0 mmol/L.毒性药理剂量组5.0 mmol/L,分别刺激细胞6 h,用1.0 mmol/L Hcy刺激内皮细胞1、6、24 h;收集细胞提取总RNA,逆转录聚合酶链反应(RT-PCR)测定Hcy对MCP-1 mRNA的表达情况.结果:不同浓度Hcy刺激CRL-1730 6 h,细胞内MCP-1 mRNA表达差异有统计学意义(P < 0.05).与生理剂量组相比,非毒性药理剂量组MCP-1 mRNA表达升高,毒性药理剂量组表达降低;1.0 mmol/L Hcy刺激CRL-1730不同时间后,MCP-1 mRNA表达随刺激时间延长呈逐渐降低的趋势,24 h表达量最低(P < 0.01).结论:Hcy可以影响人脐静脉内皮细胞MCP-1 mRNA的表达,在动脉粥样硬化的发生过程中发挥重要的作用.     

二苯乙烯苷对H_2O_2诱导血管内皮细胞黏附分子表达的影响

目的研究二苯乙烯苷(TSG)对过氧化氢(H2O2)诱导损伤的人脐静脉内皮细胞P-selectin、E-selectin、ICAM-1、VCAM-1和MCP-1表达的影响。方法体外培养人脐静脉内皮细胞,实验分为空白对照组、H2O2组、辛伐他汀组、TSG组,运用逆转录聚合酶链式反应和酶联免疫吸附试验分别检测P-selectin、E-selectin、ICAM-1、VCAM-1和MCP-1 mRNA与蛋白的表达。结果 200μmol·L-1的H2O2作用内皮细胞24 h后,P-selectin、E-selectin、ICAM-1、VCAM-1和MCP-1的mRNA和蛋白表达水平均明显上调;经TSG预处理内皮细胞4 h后,再加200μmol·L-1的H2O2作用内皮细胞24 h,结果显示:TSG能抑制H2O2诱导的内皮细胞P-selnecti、E-se-lectin、ICAM-1、VCAM-1和MCP-1的mRNA和蛋白的表达。结论 TSG可抑制H2O2诱导的人脐静脉内皮细胞黏附分子的表达。     

糖皮质激素联合环磷酰胺对人脐静脉内皮细胞增殖及其细胞间黏附分子-1和单核细胞趋化因子-1表达水平的影响

目的：探讨地塞米松、环磷酰胺对人脐静脉内皮细胞（Human umbilical vein endothelial cells,HUVECs）细胞增殖及其细胞间粘附分子-1（ICAM-1）和单核细胞趋化因子-1（MCP-1）基因表达的影响。方法：对培养的人脐静脉内皮细胞,在不同时间以不同药物浓度分别加入地塞米松和环磷酰胺进行干预。以MTT法检测药物对脐静脉内皮细胞增殖的影响。计算出两种药物的半数抑制浓度（IC50）。以地塞米松和环磷酰胺半数抑制浓度分别及联合作用血管内皮细胞48h,以RT-PCR的方法比较三组间血管内皮细胞ICAM-1和MCP-1的mRNA表达差异。结果：1、地塞米松、环磷酰胺均呈时间、剂量依赖性地抑制HUVECs细胞的增殖,地塞米松和环磷酰胺IC50分别为0.74 mg/ml、1.87mg/ml。2、脐静脉内皮细胞在地塞米松和环磷酰胺分别及联合孵育下,人脐静脉内皮细胞ICAM-1和MCP-1 mRNA表达水平较对照组显著下降（p〈0.05）,且联合作用组显著低于单个药物组（p〈0.05）。结论：糖皮质激素和环磷酰胺抑制血管内皮细胞增生,并抑制血管内皮细胞ICAM-1和MCP-1 mRNA表达,从而对血管起到保护作用。为临床治疗血管炎提供理论支持。     

α-硫辛酸对AGEs作用下血管内皮细胞PD-L1表达的影响

目的探讨α-硫辛酸(LA)对糖基化终产物(AGEs)作用下的人脐静脉血管内皮细胞株(HUVEC)表面程序性死亡配体1(PD-L1)分子表达及培养上清液中可溶性PD-L1(sPD-L1)浓度的影响。方法实验分四组:正常对照组(C组:RPMI1640培养);糖基化牛血清白蛋白(AGE-BSA)组[培养液分别为AGE-BSA50mg/ml(AG50组)、200mg/ml(AG200组)和400mg/ml(AG400组)];牛血清白蛋白(BSA)对照组[培养液分别为BSA50mg/ml(BG50组)、200mg/ml(BG200组)和400mg/ml(BG400组)];药物干预组[培养液分别为RPMI1640+200μmol/LLA(C+LA200组)、200mg/mlAGE-BSA+200μmol/LLA(AG200+LA200组)]。孵育72h后,检测各组HUVEC细胞表面PD-L1的表达及上清液中sPD-L1浓度的变化。结果不同浓度AGE-BSA作用细胞72h,PD-L1的表达及sPD-L1浓度较对照组显著升高(P<0.01),其效应呈现一定的浓度依赖性。在LA干预下,AG200+LA200组PD-L1表达及s...     

Celecoxib modulates adhesion of HT29 colon cancer cells to vascular endothelial cells by inhibiting ICAM-1 and VCAM-1 expression

BACKGROUND AND PURPOSE: Cyclooxygenase-2 (COX-2) is highly expressed during inflammation and can promote the progression of colorectal cancer. Interactions between cancer cells and vascular endothelial cells are key events in this process. Recently, the selective COX-2 inhibitor, celecoxib, was shown to inhibit expression of the adhesion molecules, ICAM-1 and VCAM-1, in the human colon cancer cell line HT29 and to inhibit adhesion of HT29 cells to FCS-coated plastic wells. Here, we evaluated the effects of celecoxib on adhesion of HT29 cells to human umbilical vein endothelial cells (HUVEC), mediated by ICAM-1 and VCAM-1, to assess further the potential protective effects of celecoxib on cancer development. EXPERIMENTAL APPROACH: Celecoxib was incubated for 4 h with HT29 cells and HUVEC and adhesion was quantified by a computerized micro-imaging system. Expression analysis of ICAM-1 and VCAM-1 cell adhesion molecules was performed by western blot. KEY RESULTS: Celecoxib (1 nM-10 microM) inhibited, with the same potency, adhesion of HT29 cells to resting HUVEC or to HUVEC stimulated by tumour necrosis factor-alpha (TNF-alpha), mimicking inflammatory conditions. Analysis of ICAM-1 and VCAM-1 expression showed that celecoxib inhibited expression of both molecules in TNF-alpha-stimulated HUVEC, but not in resting HUVEC; inhibition was concentration-dependent and maximal (about 50%) at 10 microM celecoxib. CONCLUSIONS AND IMPLICATIONS: In conclusion, our data show that celecoxib inhibits HT29 cell adhesion to HUVEC and expression of ICAM-1 and VCAM-1, in stimulated endothelial cells. These effects may contribute to the chemopreventive activity of celecoxib in the development of colorectal cancer.     

丹参酮Ⅱ—A磺酸钠对内皮细胞和血小板体外表达粘附分子的作用

AIM: To study the action of tanshinone II-A sulfonate (Tan) on adhesion molecule expression by cultured endothelial cells and platelets. METHODS: Tumor necrosis factor alpha (TNF-alpha)-induced ICAM-1 expression on the cell surface and endothelial adhesivity toward HL-60 cells were studied using human umbilical vein endothelial cells (HUVEC). Thrombin-induced expression of platelet P-selectin was studied using human blood platelets. Adhesion molecule expression on the cell surface was measured by flow cytometry. The number of HL-60 cells adhering to the HUVEC monolayer was determined by liquid scintillation spectroscopy. RESULTS: Pretreatment of HUVEC with TNF-alpha significantly enhanced ICAM-1 expression and increased HL-60 cells adhesion to HUVEC from 4.6% +/- 0.7% to 30% +/- 6%. Tan (25-200 mumol.L-1) inhibited the effects of TNF-alpha in a concentration-dependent manner. Tan also inhibited the increase of P-selectin expression of thrombin-activated platelets in a concentration-dependent manner. CONCLUSION: Tan inhibited expression of adhesion molecules (ICAM-1, P-selectin) in HUVEC and in human blood platelets.     

Regulation of endothelin-1 production in deoxycorticosterone acetate- salt-treated endothelial cells

The aim of this study was to investigate the direct effect of deoxycorticosterone acetate (DOCA) on the expression of endothelin-1 (ET-1) mRNA and production of ET-1 peptides in cultured bovine carotid endothelial cells (BCEC) and human umbilical vein endothelial cells (HUVEC). The mineralocorticoid, DOCA, was administered to BCEC and HUVEC with or without additional salt (200 mmol/l). The ET-1 mRNA was elevated to 150% and 180% after a 24-hour incubation with DOCA (5 micromol/l) in BCEC and HUVEC, respectively. Intracellular content of ET-1 peptides of BCEC and HUVEC was increased from 21.66 +/- 0.3 to 23.64 +/- 0.19 fmol/10(5) cells and from 8.38 +/- 0.82 to 11.26 +/- 0.91 fmol/10(5) cells, respectively, in the DOCA-conditioned medium. Also, DOCA treatment for 24 h increased the secretion of ET-1 peptide from 1.62 +/- 0.17 to 5.33 +/- 0.67 fmol/10(5) cells in BCEC and from 0.95 +/- 0.08 to 3.56 +/- 0.36 fmol/10(5) cells in HUVEC. In DOCA-salt-treated endothelium, regulation of ET-1 gene was similar to that with DOCA alone. The DOCA-induced increase in expression of ET-1 mRNA and the ET-1 peptide level were both diminished in dexamethasone (DEX, 10 nmol/l)- or mifepristone (RU486, 0.5 micromol/l)-treated endothelium. These results suggest that DOCA directly increased the ET-1 mRNA expression in endothelium and could be mediated in part by a glucocorticoid receptor pathway which was independent of salt and hyperosmolarity.     

总丹酚酸对过氧化氢诱导内皮细胞损伤的抑制作用(英文)

目的　研究总丹酚酸对过氧化氢 (H2 O2 )诱导血管内皮细胞损伤的影响。方法　培养的人脐静脉内皮细胞 ,用MTT法测定内皮细胞的存活率。用碘化丙啶 (PI)染色和TUNEL法测定H2 O2 诱导内皮细胞的凋亡作用。用荧光法测定半胱天冬酶 (cas pase) 3的活性。用Fura 2 /AM测定内皮细胞内游离钙离子浓度 ([Ca2 + ] i)。结果　 1 0 0 μmol·L-1 H2 O2可使内皮细胞的存活率下降 40 .2 % ,提前 1h给予总丹酚酸 1 0和 1 0 0mg·L-1 使存活率分别增加8.4%和2 8.6 %。 1 0 0 μmol·L-1 H2 O2 还可引起内皮细胞的凋亡 ,PI染色的结果显示 ,H2 O2 处理内皮细胞 1 8h后 ,凋亡率从 (7.1 %± 0 .7) %升至 (38.1±4.0 ) %。总丹酚酸 1 0 0mg·L-1 提前处理内皮细胞1h,可使内皮细胞凋亡率降至 (1 3 .6± 0 .8) %。TUNEL方法检测结果显示 ,H2 O2 处理内皮细胞后 ,TUNEL染色阳性的细胞从 (3 .0± 0 .8) %升至 (30 .5±2 .9) % ,总丹酚酸 1 0 0mg·L-1 可使TUNEL阳性细胞率降至 (1 9.0± 3 .7) %。此外 ,H2 O2 处理细胞后 ,内皮细胞半胱天冬酶 3的活性增加 1 76% ,[Ca2 + ] i 升高 1 0 1 % ,而总丹酚酸可以抑制H2 O2 引起的半胱天冬酶 3活性的增加和 [Ca2 + ] i 升高。结论　总丹酚酸对H2 O2 引起的内皮细胞损伤具有明显的抑制作     

川崎病急性期血清对血管内皮MMP-2、MMP-9和TNF-α分泌的影响及IVIG的干预机制探讨

目的：观察川崎病（Kawasaki disease,KD）患儿急性期血清对脐静脉内皮细胞（HUVEC）分泌基质金属蛋白酶-2（matrix metalloproteases-2,MMP-2）、基质金属蛋白酶-9（matrix metalloproteases-9,MMPO）和TNF-α的影响及人血丙种球蛋白（IVIG）对上述过程的调节作用。方法：HUVEC培养分为正常血清组（C组）、发热血清组（F组）、川崎病冠脉无损害血清组（NAC组）、川崎病冠脉无损害血清4-IVIG组（NACI组）、川崎病冠脉损害血清组（AC组）、川崎病冠脉损害血清＋WIG组（ACI组）。每组分别培养12h后吸取上清液,应用ELISA法测定细胞上清液MMP-2、MMP-9和TNF-α水平。结果：经川崎病患儿血清作用后的HUVEC培养上清液中MMP．2、MMP．9和TNF-α水平升高明显,与C组、F组相比差异有统计学意义（P均〈0．01）,其中AC组更高,与NAC纽相比差异有统计学意义（P〈0．01）;F组上清液中MMP-2、MMP-9和TNF-α水平虽然低于川崎病组,但仍高于C组（P〈0．01）。经丙种球蛋白干预后,AC组、NAC组MMP-2、MMP-9和TNF-α水平下降,差异有统计学意义（P均〈0．01）。HUVEC培养上清液中MMP-2、MMP-9与TNF-α含量之间呈显著性正相关（r=0．839,0．765,P〈0．01）。结论：川崎病患儿急性期血清能诱导HUVEC分泌MMP-2、MMP-9和TNF-α增加,MMP-2、MMP-9和TNF-α可能参与川崎病患儿冠脉损害的发生发展;IVIG防治冠脉损害的机制,可能与抑制内皮细胞分泌MMP-2、MMP-9和TNF-α有关。     

3,4-oxo-isopropylidene-shikimic acid inhibits adhesion of polymorphonuclear leukocyte to TNF-α-induced endothelial cells in vitro

AIM：To examine the effect of 3,4-oxo-isopropylidene-shikimic acid (ISA) on human polymorphonuclear leukocyte (PMN) adhesion to human umbilical vein endothelial cells (HUVEC) and explore its mechanism. METHODS:Adhesion of PMN to HUVEC was measured by rose bengal staining assay. Cell-EL1SA and RT-PCR methods were used to examine the expression of adhesion molecules ICAM-1. Cell viability was detected with MTT assay.RESULTS: ISA (1-100μmol/L) effectively reduced PMN adhesion to TNF-α-induced HUVEC with the inhibitory rate from 17.2% to 53.5%, and exerted no effect on PMN adhesion to normal HUVEC. Adhesion molecule ICAM-1 surface protein and mRNA expression induced by TNF-α (400kU/L) were significantly inhibited by ISA. In addition, the cell viability of HUVEC was unchanged 48h after treatment with ISA. CONCLUSION: ISA inhibited TNF-α-stimulated PMN-HUVEC adhesion and expression of ICAM-1.     

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   

高晶体-高胶体渗透压混合液对缺氧/氧再灌损伤的内皮细胞容积和存活率的影响

目的 :观察高晶体 高胶体渗透压混合液(HHS)对缺氧 氧再灌损伤的人脐静脉内皮细胞(HUVEC)容积和存活率的影响。方法 :取HUVEC株ECV 30 4 ,分为对照组和实验组。两组细胞先置于缺氧 (95 %氮气 ,5 %CO2 )环境中 8h ,然后将实验组细胞置于HHS 15min ,再在常氧状态下 (95 %空气 ,5 %CO2 )培养 16h。对照组细胞直接置于常氧状态下 (95 %空气 ,5 %CO2 )培养 16h。两组细胞分别于实验前、实验开始后 15、6 0min和 8、8.2 5、16及2 4h测其细胞容积和存活率。结果 :对照组细胞在缺氧 6 0min后及氧再灌过程中明显肿胀 (P <0 .0 5或 0 .0 1) ,细胞存活率进行性降低 (P <0 .0 5或 0 .0 1)。实验组细胞经HHS处理后细胞容积较同一时段的对照组细胞容积明显缩小 (P <0 .0 1) ,存活率尽管仍低于实验前 (P <0 .0 1) ,但明显高于同一时段的对照组 (P <0 .0 5 )。结论 :HHS具有刺激内皮细胞产生延迟性调节性容积减少 ,保持容积稳定的作用 ,能在一定程度上降低内皮细胞的死亡率 ,保护缺氧 氧再灌损伤的内皮细胞。     

Inhibitory effects of bucillamine on the expression of vascular cell adhesion molecule-1 in human umbilical vein endothelial cells

Bucillamine (BUC) has been found to have beneficial effects in the treatment of rheumatoid arthritis (RA), in which the activation of endothelial cells plays an important role in the pathogenesis. The current studies examined the effect of BUC and its intramolecular disulfide form (BUC-ID) on the expression of adhesion molecules in human umbilical vein endothelial cells (HUVEC) stimulated with tumor necrosis factor-alpha (TNF-alpha). HUVEC (4 x 10(4)/well) were incubated with medium M199 containing heparin and 20% FCS with endothelial cell growth supplement (ECGS) for 24 h in the presence or absence of BUC or BUC-ID, after which the culture medium was replaced with ECGS free medium. Then the cultures were further carried out for additional 24 h with TNF-alpha (10 ng/ml) in the presence or absence of BUC or BUC-ID. BUC-ID, but not BUC, appeared to suppress the expression of VCAM-1 on HUVEC stimulated with TNF-alpha in a dose-response manner at its pharmacologically relevant concentrations (0.3-3.0 microg/ml), whereas only the 3 microg/ml concentration level of BUC-ID had a statistically significant effect, although the effect was relatively small. By contrast, lower concentrations of BUC-ID (1-3 microg/ml) suppressed the secretion of soluble VCAM-1 by HUVEC much more effectively. Of note, at the concentration of 3 microg/ml neither BUC nor BUC-ID significantly influenced the expression of ICAM-1 and E-selectin on TNF-alpha stimulated HUVEC. These results indicate that BUC-ID, but not BUC, specifically downregulates the surface expression of VCAM-1 as well as the release of soluble VCAM-1 by HUVEC stimulated with TNF-alpha. BUC-ID suppressed the production of solubleVCAM-1 by RA bone marrow CD34+ cells stimulated with SCF, GM-CSF and TNF-alpha more effectively than BUC. The data thus suggest that one of the mechanisms of action of BUC involves the inhibition of the activation of endothelial cells.