细胞黏附分子与子痫前期发病关系的研究

目的 检测子痫前期患者和正常孕妇胎盘组织中血管细胞黏附分子-1(VCAM-1)、细胞间黏附分子-1(ICAM-1)及血小板内皮细胞黏附分子-1(PECAM-1)的表达水平,以探讨细胞黏附分子(CAM)在子痫前期发病机制中的作用.方法 选取2005年5月-2006年5月在郑州大学第三附属医院住院分娩病例80例,分为3组:①轻度子痫前期组20例;②重度子痫前期组30例;③正常晚孕组(NT组)30例;胎盘组织中MCAM-1、ICAM-1及PECAM-1的表达水平采用免疫组化PV-9000法测定.结果 ①重度子痫前期组胎盘组织中VCAM-1和PECAM-1的表达下降(P＜0.05),ICAM-1的表达增强(P＜0.05).②轻度子痫前期组胎盘组织中VCAM-1的表达下降(P＜0.05).ICAM-1和PECAM-1的表达无明显差异(P＜0.05).结论 CAM与子痫前期发病有密切联系,VCAM-1、ICAM-1和PECAM-1参入了子痫前期病理生理过程且与子痫前期的病情程度密切相关.     

丹皮酚抑制大鼠局灶性脑缺血再灌注损伤脑组织细胞间黏附分子-1和血管细胞黏附分子-1的表达

目的观察丹皮酚对大鼠脑缺血再灌注损伤后脑组织细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)表达的影响,以探讨其脑保护的作用机制。方法线栓法制备大鼠局灶性脑缺血再灌注损伤模型,大鼠脑缺血2 h再灌注24 h,采用Western blot及RT-PCR法观察大鼠脑组织ICAM-1、VCAM-1的蛋白及mRNA表达。结果丹皮酚明显降低缺血区脑组织ICAM-1、VCAM-1的蛋白及mRNA的表达。结论丹皮酚可能通过降低缺血区脑组织黏附分子表达发挥脑保护作用。     

支气管哮喘血清可溶性细胞间黏附分子-1和内皮细胞黏附分子-1的表达

目的　探讨可溶性细胞间黏附分子 - 1(s ICAM- 1)和血管内皮细胞黏附分子 - 1(s VCAM- 1)在支气管哮喘发病中的意义。方法　对支气管哮喘患者 2 3例和健康人 2 0名 (年龄均在 15～ 45岁之间 ) ,采用酶联免疫双抗体夹心法 (EL ISA)测定血清中的 s ICAM- 1和 s VCAM- 1;利用荧光酶联免疫法 (Uni- CAP系统 )分析血清中总 Ig E(t Ig E)和特异性 Ig E(s Ig E)。结果　血清 s ICAM- 1、s VCAM- 1、t Ig E水平测定哮喘组均高于对照组 (P<0 .0 1) ;血清中以户尘螨和蒿草花粉的特异性 Ig E含量增高为主 ;经多元逐步回归分析提示血清总 Ig E含量与s ICAM- 1存在线性关系 ,其复相关平方 (R- square)为 0 .5 0 2 ,标准偏回归系数为 0 .0 97,t=2 .841,P=0 .0 2 18。结论　支气管哮喘患者的 s ICAM- 1和 s VCAM- 1含量显著高于正常人 ;血清 s ICAM- 1与血清总 Ig E存在线性依存关系。     

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。     

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。     

急性白血病患者中ICAM-1和VCAM-1的表达及意义

目的 探讨细胞间黏附分子1(ICAM-1)和血管细胞间黏附分子1(VCAM-1)在急性白血病(AL)中的表达及临床意义.方法 39例初诊AL患者,其中27例经治疗后达完全缓解(CR).采用逆转录-PCR法检测AL骨髓单个核细胞ICAM-1和VCAM-1的mRNA表达水平.对照组12例均为骨髓像正常的门诊患者.结果 ICAM-1和VCAM-1水平在初诊AL者明显高于CR组及对照组(P＜0.01),且CR组和对照组之间无显著差异(P＞0.05);高白细胞(WBC＞100×109/L)组和死亡组的ICAM-1和VCAM-1水平明显增高(P＜0.05).髓外浸润组仅ICAM-1高于非髓外浸润组(P＜0.01);非淋巴细胞AL(ANLL)具有良好核型者ICAM-1水平低于其他患者(P＜0.05).结论 AL表达ICAM-1和VCAM-1明显增高,其检测对疗效及预后判断有重要意义.     

狼疮性肾炎患者外周血细胞间黏附分子-1和P-选择素的表达

目的 观察细胞间黏附分子-1(ICAM-1)和P-选择素在狼疮性肾炎(LN)患者外周血中的表达水平.方法 用ELISA方法分析了36例LN患者和11例正常人外周血ICAM-1和P-选择素表达情况.结果 LN患者外周血ICAM-1和P-选择素表达与正常对照组比较有明显差异(P＜0.05).结论 ICAM-1和P-选择素表达与LN的病变有一定相关性.     

血管细胞黏附分子-1与动脉粥样硬化机制的研究现状北大核心CSCD

动脉粥样硬化(AS)是一种慢性的、以脂质发育为特征的炎症过程。血管细胞黏附分子-1(VCAM-1)是一种炎症因子,表达在炎症环境下的内皮细胞膜上,介导白细胞的滚动和黏附。在AS开始初期,免疫细胞和脂质浸润血管壁形成斑块,VCAM-1在这个过程中发挥了重要的作用。本文对目前AS发生、发展过程中VCAM-1高表达的诱因及其病理机制,以及通过减少VCAM-1表达抗AS的药物进行了综述。     

羟苯磺酸钙对糖尿病大鼠肾脏表达ICAM-1和VCAM-1的影响

目的:探讨羟苯磺酸钙对肾小球细胞间黏附分子(ICAM-1)和血管细胞黏附分子(VCAM-1)表达的影响和对糖尿病肾病的保护作用.方法:左肾切除后单次腹腔注射50mg·kg-1链脲佐菌素制备糖尿病大鼠模型,糖尿病大鼠随机分成糖尿病组、羟苯磺酸钙治疗组(100 mg·kg-1·d-1)和正常对照组.用RT-PCR及Western印迹的方法检测12周后ICAM-1、VCAM-1表达的改变.结果:与正常对照组相比,糖尿病组及治疗组ICAM-1、VCAM-1表达增加(P＜0.01);而治疗组ICAM-1、VCAM-1表达显著低于糖尿病组(P＜0.01).结论:羟苯磺酸钙可抑制糖尿病大鼠ICAM-1和VCAM-1的表达,延缓糖尿病肾病的发生、发展.     

核因子κB肿瘤坏死因子-α和细胞间黏附分子-1在特发性黄斑前膜中的表达及临床意义

目的研究特发性黄斑前膜(IMEM)组织中核因子(NF)-kB、肿瘤坏死因子(TNF)-α、细胞间黏附分子(ICAM)-1的表达及其作用。方法用免疫荧光法检测12例IMEM组织和9名正常黄斑区内界膜组织中NF-kB、TNF-α、ICAM-1的表达。结果NF-kB、TNF-α、ICAM-1的阳性表达分别为8例(67%)、10例(83%)、9例(75%),对照组正常黄斑区内界膜组织3种细胞因子未见明显阳性荧光染色。结论NF-kB、TNF-α和ICAM-1介导的炎症反应在IMEM发生中具有一定作用。     

IL-6在早孕绒毛蜕膜中的表达及米非司酮对其的影响

目的观察IL-6在早孕绒毛、蜕膜组织中的表达及米非司酮对其表达的影响,探讨药物流产的分子免疫作用机制。方法采用免疫组化染色测定早孕绒毛及蜕膜组织中IL-6的表达,其中正常早孕人工流产组20例,米非司酮药物流产组22例。结果IL-6在正常早孕绒毛及蜕膜组织中均呈阳性表达,米非司酮药物流产组表达强度明显降低(P<0.01)。结论IL-6在早孕绒毛及蜕膜中有较高水平表达,可能与胚泡着床、妊娠维持有关,米非司酮明显降低其表达,影响胚胎发育引起流产。     

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。     

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   

Motorcycle exhaust particles up-regulate expression of vascular adhesion molecule-1 and intercellular adhesion molecule-1 in human umbilical vein endothelial cells

Epidemiological studies have shown that there is a strong correlation between atherosclerosis and ambient air pollution. In this study, we found that motorcycle exhaust particles (MEP) induced adhesion between cells of the human monocytic leukemia cell line (THP-1) and human umbilical vein endothelial cells (HUVECs) in a time-and dose-dependent manner. In addition, MEP treatment induced both mRNA and protein expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) in HUVECs. The IκB degradation and p65 nuclear translocation was found in MEP-treated HUVECs, suggested the involvement of nuclear factor-κB (NF-κB). MEP-induced VCAM-1 and ICAM-1 protein expression was inhibited by NF-κB inhibitor BAY 11-7085. Oxidative stress was also involved in the signaling of VCAM-1 and ICAM-1 expression. MEP treatment caused hydrogen peroxide and superoxide formation. Pretreatment with α-tocopherol could inhibit MEP-induced reactive oxygen intermediates generation and suppressed MEP-induced IκB degradation and adhesion molecules expression. Furthermore, the carbon black (CB) nanoparticles with different diameters could induce VCAM-1 and ICAM-1 protein expression; however, polycyclic aromatic hydrocarbons (PAHs) only increased the expression of ICAM-1 but not that of VCAM-1 in HUVECs. In this study, we found that MEPs could induce ICAM-1 and VCAM-1 expression through oxidative stress and NF-κB activation in HUVECs.     

Influence of natural and synthetic compounds on cell surface expression of cell adhesion molecules, ICAM-1 and VCAM-1

Various natural and synthetic compounds including alkaloids, terpenoids and phenolics were tested for inhibition of the cell surface expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), both of which are crucial in the regulation of immune response and inflammation. Of 40 compounds tested, two compounds significantly downregulated the expression of VCAM-1 on murine endothelial cells (F-2) and ten compounds that of ICAM-1 on mouse myeloid leukemia cells (M1). Sanguinarine chloride (5) and isoliquiritigenin (13) were capable of lowering the levels of both ICAM-1 and VCAM-1. The structure-activity relationships study on chalcone and flavone derivatives related to 13 suggested that the inhibitory activity of the chalcone derivatives is attributable to the 4-hydroxy group as well as the possible coplanarity between the phenyl ring and the adjacent conjugated ketone.     

Tanshinone IIA inhibits TNF-α-mediated induction of VCAM-1 but not ICAM-1 through the regulation of GATA-6 and IRF-1

The goal of this study was to investigate the differential effect of tanshinone IIA on the induction of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) by TNF-α and the possible molecular mechanisms by which it regulates ICAM-1 and VCAM-1 expression differentially. Stimulation of human umbilical vein endothelial cells (HUVEC) with TNF-α increased ICAM-1 and VCAM-1 expressions, and the pretreatment with tanshinone IIA concentration dependently inhibited VCAM-1 expression but not ICAM-1 expression. In previous study, PI3K/Akt, PKC and Jak/STAT-3 pathways were involved in the TNF-α-mediated induction of VCAM-1 but not ICAM-1. Thus, we examined the effect of tanshinone IIA on TNF-α-mediated activations of PI3K/Akt, PKC and Jak/STAT-3 pathways. Tanshinone IIA efficiently inhibited the phosphorylations of Akt, PKC and STAT-3 by TNF-α. Moreover, we determined the effect of tanshinone IIA on IRF-1 or GATAs induction and binding activity to VCAM-1 promoter since the upstream promoter region of VCAM-1 but not ICAM-1 contains IRF-1 and GATA binding motifs. Western blot analysis and ChIP assay showed that tanshinone IIA efficiently inhibited TNF-α-increased nuclear level of IRF-1 and GATA-6 and their binding affinity to VCAM-1 promoter region. Taken together, tanshinone IIA selectively inhibits TNF-α-mediated expression of VCAM-1 but not ICAM-1 through modulation of PI3/Akt, PKC and Jak/STAT-3 pathway as well as IRF-1 and GATA-6 binding activity.     

Inhibition of γ-irradiation induced adhesion molecules and NO production by alginate in human endothelial cells

Inflammation is a frequent radiation-induced reaction following therapeutic irradiation. Treatment of human umbilical endothelial cells (HUVEC) with gamma-irradiation (gammaIR) induces the expression of adhesion proteins such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Since the upregulation of these proteins on endothelial cell surface has been known to be associated with inflammation, interfering with the expression of adhesion molecules is an important therapeutic target. In the present study, we demonstrate that high mannuronic acid-containing alginate (HMA) inhibits gammaIR induced expression of ICAM-1, VCAM-1, and E-selectin on HUVEC in a dose dependent manner. HMA also inhibited gammaIR induced production of Nitric oxide (NO). These data suggest that HMA has therapeutic potential for the treatment of various inflammatory disorder associated with an increase of endothelial leukocyte adhesion molecules.     

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.     

Cryptotanshinone attenuates in vitro oxLDL-induced pre-lesional atherosclerotic events

Development of early stage atherosclerosis involves the activation of endothelial cells by oxidized low-density lipoprotein (oxLDL) with subsequent increases in endothelial permeability and expression of adhesion molecules favoring the adherence of monocytes to the endothelium. Cryptotanshinone (CTS), a major compound derived from the Chinese herb Salvia miltiorrhiza, is known for its protective effects against cardiovascular diseases. The aim of this study was to determine whether CTS could prevent the oxLDL-induced early atherosclerotic events. OxLDL (100?μg/mL) was used to increase endothelial permeability and induce monocyte-endothelial cell adhesion in human umbilical vein endothelial cells (HUVECs). Endothelial nitric oxide (NO) concentrations, a permeability-regulating molecule, and expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were measured. Results show that a) endothelial hyperpermeability was suppressed by 94?% (p?相似文献