细胞间粘附分子-1在大鼠肾缺血再灌注中的表达

观察肾缺血再灌注过程中，细胞间粘附分子-l(ICAM-1)在肾组织中的表达。大鼠随机分正常组和缺血再灌注模型组，应用免疫组化方法检测肾组织中ICAM-l的表达，经图象分析定量正常对照组和模型组(肾缺血lh，再灌注24、48、72和96h)ICAM-1的表达水平。正常组肾组织未见ICAM-l表达，模型组大鼠肾缺血1h未再灌注时亦未见ICAM-1的表达，再灌注24h出现明显的ICAM-1表达，48～72h达高峰，并持续至96h。提示ICAM-1介导并参与了肾缺血再灌注的损伤机制。     

细胞间黏附分子-1抑制参与大鼠小肠缺血后处理的保护作用

目的观察缺血后处理（I-postC）对缺血／再灌注（I／R）大鼠小肠组织细胞间黏附分子-1（ICAM-1）表达和髓过氧化物酶（MPO）活性的影响，探讨其减轻I／R损伤的机制。方法32只健康雄性Wistar大鼠随机分为假手术（Sham）、I／R、I-postC及缺血预处理（IPC）组，以无创动脉夹夹闭肠系膜上动脉建立小肠I／R损伤模型，常规制备病理切片，光镜下观察肠组织损伤情况。试剂盒测定MPO、超氧化物歧化酶（SOD）活性及丙二醛（MDA）含量，免疫印迹法检测小肠组织ICAM-1和NF-κBP65的表达。结果I-postC明显减轻I／R导致的小肠组织病理变化，抑制I／R所致的小肠组织MPO活性和MDA含量升高（分别为I／R组的68．7％和77、1％，P〈0.05），上调SOD活性（为I／R组的1．2倍，P〈0.05），并下调小肠组织NF-κBP65和ICAM-1表达（分别较I／R组低44．3％和49．0％，P〈0．01）。结论I-postC通过抑制ICAM-1表达和中性粒细胞游出而减轻小肠I／R损伤。     

低分子肝素对缺血再灌注大鼠肾组织核因子-κB表达的影响

探讨低分子肝素对缺血再灌注大鼠肾组织核因子-κB（NF-κB）表达的影响。建立大鼠IRI模型，健康WistaI大鼠80只随机分为正常对照组、假手术组、模型未治疗组、LMWH治疗组，后两组又分别分为术后1、3、6、24h组。检测各组血清肌酐（Scr）水平及中性粒细胞（PMNs）细胞间黏附分子-1（ICAM-1）表达；通过光镜和免疫组织化学方法观察各组大鼠肾组织形态学及趋化因子NF-κB表达变化。结果表明：（1）肾缺血再灌注未治疗组造模后1h，Scr水平虽然没有明显变化，但ICAM-1、NF-κB表达增多，肾小管坏死积分值亦较假手术组明显增加（P〈0．01）；（2）缺血再灌注6h以后，两组Scr浓度明显增高（P〈0．01），但LMWH治疗组SCr、ICAM-1、NF-κB表达水平及肾小管坏死积分值均明显低于模型未治疗组（P〈0．05）；（3）肾组织中NF-κB表达与肾小管损伤积分值呈现良好的相关性（r=0．71，P〈0、01）；而NF-κB与ICAM-1间则呈现显著正相关（r=0．62，P〈0．05）。由此说明：（1）ICAM-1、NF-κB在肾缺血再灌注早期的瞬时表达，可能参与了炎症早期的白细胞迁移与浸润，与肾损伤的发生密切相关；（2）LMWH可通过减少ICAM-1及NF-κB的表达，阻抑炎症反应过程，减轻肾组织损伤。     

黏附分子与树突状细胞在大鼠肝和肾缺血-再灌注损伤中作用及抗黏附干预的影响

目的本研究旨在探讨黏附分子P -选择素、ICAM -1及DC在大鼠肝和肾缺血 -再灌注损伤中作用 ,以及抗P -选择素Lectin -EGF功能域单抗 (PsL -EGFmAb)的抗黏附抑制及其防治效果。方法分别建立肝和肾缺血 -再灌注损伤大鼠模型90只 ,随机将两组模型各分为P -选择素单抗治疗组 (n=20)和非治疗组 (n=20) ,按不同再灌注时间 (1 ,3,6和24h)再分为4组 ,每组5只。治疗组于再灌注前5min静脉内注射自制的PsL-EGFmAb,剂量为2mg/kg。另各设假手术组(n=5)作为对照。采用免疫组化LSAB法和免疫双染与荧光图像分析法 ,分别观察和比较各组大鼠肝、肾组织P -选择素、ICAM -1表达及CD1a CD80 DC分布变化。结果①缺血 -再灌注1h起 ,伴随着肝、肾组织病理学改变 ,P -选择素即分别以肝窦内皮细胞或肾小管上皮细胞为主于肝和肾内广泛高表达 ,至24h仍维持一定水平。ICAM -1于缺血 -再灌注6h起持续以肝窦和肾血管为主表达上调和明显增强。②CD1a CD80 DC在假手术组大鼠肝、肾组织中分布甚少 ,而在非治疗组自再灌注1h起以肝窦和肾小管间质为主分布数量逐渐增多 ,至24h达峰 ,并与大鼠肝、肾功能密切相关。③经PsL -EGFmAb处理后 ,大鼠肝、肾组织P -选择素和I CAM -1表达受到抑制 ,CD1a CD80 DC分布及数量减少 ,组织病理损伤及肝、     

细胞间黏附分子-1的研究概况及临床意义

细胞间黏附分子-1( ICAM-1)是一种细胞表面的跨膜糖蛋白,可介导细胞与细胞间或细胞与细胞外基质之间的相互作用.ICAM-1广泛地参与细胞黏附、炎症的发生发展、信号转导和肿瘤转移等多种重要的生理及病理过程.在临床上,ICAM-1可作为多种炎症或肿瘤发展和预后的重要生物标记物之一.以ICAM-1为靶点的药物或能预防和治疗多种急、慢性炎症引起的组织损伤和肿瘤等.     

ICAM-1与脑缺血再灌注损伤研究进展

急性缺血性脑卒中的本质是脑血流障碍造成的脑损害．在时间窗内早期恢复血流有利于缩小梗死范围、减轻神经损害。目前早期溶栓是治疗急性缺血性脑卒中最有效的措施。但由于溶栓时间窗（≤3h）的限制，只有少数（约5％）的病人得益于溶栓治疗。同时。由于溶栓后再灌注引起的颅内出血、脑水肿等严重并发症也限制着溶栓治疗的推广应用。如何减轻再灌注损伤成为了提高急性缺血性脑卒中疗效的关键之一。许多临床试验以离子通道、氧自由基、兴奋性氨基酸受体为靶点进行神经保护性治疗。但结果令人失望，目前研究的注意力已转向与脑缺血再灌注损伤有关的炎症反应。大量证据表明。急性炎症反应在脑缺血再灌注损伤中起着重要作用。因此阻断炎症级联反应可能是改善脑缺血再灌注损伤的理想策略。脑缺血和再灌注早期产生的黏附分子、细胞因子及中性粒细胞聚集构成了炎症反应的基础。     

细胞间黏附分子-1基因多态性与疾病易感性

细胞间黏附分子-1(ICAM-1)属于免疫球蛋白超家族成员之一,是一种细胞表面单链糖蛋白,它表达于多种细胞表面,通过识别其受体LFA-1、MAC-1、P150、P95介导细胞-细胞间的黏附,参与多种炎症反应及免疫过程。不同种族和地区研究证实ICAM-1基因多态性与人类多种疾病相关。     

牛磺酸对大鼠肢体缺血再灌注后肺损伤时黏附分子ICAM-1表达的影响

目的：探讨牛磺酸对大鼠肢体缺血再灌注致肺损伤时黏附分子ICAM-1表达的影响。方法：复制大鼠肢体缺血再灌注(LIR)损伤模型,采用流式细胞技术、逆转录聚合酶链反应（RT-PCR）和Western blotting观察LIR后肺损伤发生过程中，血液中CD18阳性的多形核白细胞（PMN）百分率、肺系数（LI）与肺通透指数（LPI）、肺组织形态学的改变、肺组织ICAM-1 在mRNA和蛋白水平的变化及牛磺酸对上述指标的影响。结果：大鼠肢体缺血再灌注后LI、LPI及CD18阳性细胞数均明显增加，肺组织髓过氧化物酶（MPO）活性增加，ICAM-1表达明显升高，而提前给予牛磺酸可以明显抑制这些变化，从而对肺起一定保护作用。结论： 肺组织细胞ICAM-1表达上调及血液中CD18阳性细胞数的增加可能参与LIR后肺损伤的发生；牛磺酸可减少血液中CD18阳性细胞数，并且下调肺组织ICAM-1的表达，从而减轻肺损伤。     

细胞间黏附分子-1基因多态性与缺血性心脑血管疾病

细胞间黏附分子-1在炎症早期介导白细胞与受损内皮细胞的黏附，由于其基因多态性影响了缺血性心脑血管疾病的发生和预后，成为研究热点。本文就该研究领域的新进展做一综述。     

细胞间黏附分子-1基因多态性与疾病易感性

细胞间黏附分子-1(ICAM-1)属于免疫球蛋白超家族成员之一，是一种细胞表面单链糖蛋白，它表达于多种细胞表面，通过识别其受体LFA-1、MAC-1、P150、P95介导细胞-细胞间的黏附，参与多种炎症反应及免疫过程。不同种族和地区研究证实ICAM-1基因多态性与人类多种疾病相关。     

EXPRESSION OF ICAM-1 AND VCAM-1 IN HUMAN MALIGNANT MESOTHELIOMA

Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are cytokine-inducible adhesion molecules which recognize ligands that are highly expressed on leukocytes. Expression of ICAM-1 and VCAM-1 was investigated in tissue sections of 16 cases of malignant mesothelioma (seven epithelial, eight biphasic, and one sarcomatoid) using immunohistochemistry. Neoplastic cells were diffusely and intensely stained for ICAM-1 in all cases. VCAM-1 was detected in 14 of 16 cases. The percentage of VCAM-1-positive tumour cells was more than 50 per cent in eight cases and the staining was observed mainly in epithelial-like cells. VCAM-1 was rarely expressed in other malignant tumours of epithelial origin, being present in only 1 of 58 cases of carcinoma originating from different anatomical sites. At the cellular level, ICAM-1 and VCAM-1 appeared co-distributed, the staining for both being cytoplasmic with a membrane reinforcement. The regulation of VCAM-1 expression by neoplastic mesothelial cells was investigated in vitro using 14 mesothelioma cell lines. ICAM-1 was expressed by cultured cells of all mesothelioma cell lines, even in the absence of cytokines. VCAM-1 was detected in 10–50 per cent of the cells in three non-stimulated mesothelioma cell lines (mero-95, mero-96, and mero-134), and was absent or poorly expressed in the remaining 11. Exposure of a negative cell line (mero-48a) to an optimal concentration of tumour necrosis factor alpha (TNFα) or interleukin-13 (IL-13) for 6–18 h resulted in the induction of VCAM-1 mRNA synthesis and in VCAM-1 expression at the membrane level in 60–70 per cent of the cells. These findings are consistent with the possibility that TNFα, IL-13, or other activating signals are released in the tumour micro-environment and regulate the expression of VCAM-1 in malignant mesothelioma cells.     

ICAM-1和VCAM-1参与脑胶质瘤侵袭生长

目的探讨脑胶质瘤向周围正常脑组织的侵袭生长与细胞间黏附分子-1(ICAM-1)及血管-细胞黏附分子-1(VCAM-1)的关系。方法共收集44例脑胶质瘤病例,取瘤周组织、肿瘤中心和正常脑组织标本,分别用免疫组化(IHC)、反转录PCR(RT-PCR)和蛋白免疫印迹(Western blot)法检测ICAM-1及VCAM-1在3组标本中的表达量。结果瘤周组织、肿瘤中心组织及正常脑组织比较ICAM-1及VCAM-1表达有显著差异(P0.05);当进行组间两两比较时有显著差异(P0.01),瘤周组织中表达量最高,肿瘤中心组织次之,正常脑组织最少,将标本分为LGGs组和HGGs组后进行比较可得出同样结论。结论 ICAM-1和VCAM-1与脑胶质瘤向周围正常脑组织的侵袭生长有密切关系。     

缺氧和高糖对大鼠肾成纤维细胞ICAM-1mRNA表达的影响

目的:探讨缺氧和高糖对肾成纤维细胞(NRK)细胞间粘附分子-1(ICAM-1)mRNA表达的影响。方法:将大鼠NRK分6组进行体外培养:(1)正常浓度葡萄糖组(常糖组):5.6mmol/L葡萄糖;(2)常糖+缺氧组:5.6mmol/L的葡萄糖+100μmol/L的CoCl2;(3)高糖A组:15mmol/L葡萄糖;(4)高糖+缺氧A组:15mmol/L葡萄糖+100μmol/L的CoCl2;(5)高糖B组:30mmol/L葡萄糖;(6)高糖+缺氧B组:30mmol/L葡萄糖+100μmol/L的CoCl2。分别于24h、48h取各组NRK采用RT-PCR检测ICAM-1mRNA表达水平。结果:与常糖组相比,高糖A组,高糖B组ICAM-1mRNA表达量逐渐升高(P<0.01),常糖+缺氧组、高糖+缺氧A、B组ICAM-1mRNA表达量也升高(P<0.01);高糖+缺氧A、B组ICAM-1mRNA表达量分别比高糖A、B组明显升高(P<0.01);高糖A、B组和常糖+缺氧组、高糖+缺氧A、B组48hICAM-1mRNA表达量均高于24h表达量(P<0.01)。结论:高糖和缺氧均可导致ICAM-1mRNA高表达,缺氧可能进一步增加高糖上调ICAM-1的表达。     

Elevated levels of soluble ICAM-1 in sera from patients with bronchial asthma

We measured the levels of soluble intercellular adhesion molecule-1 (sICAM-1) in sera from patients with bronchial asthma. sICAM-1 levels in sera from atopic asthmatic patients in stable conditions were higher than in normal control subjects. Furthermore, the sICAM-1 levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. These results suggest that higher levels of sICAM-1 in sera reflect the upregulation of ICAM-1 expression in allergic inflammation.     

ICAM-1在疟原虫感染红细胞与内皮细胞粘附中功能的研究进展

细胞间粘附分子1(ICAM1),又名CD54,是免疫球蛋白超家族的成员之一,是一种重要的细胞表面粘附因子。ICAM1在介导疟原虫感染红细胞(PRBC)和血管内皮细胞粘附中起到重要的作用。重症疟疾患者血管内皮细胞表面的ICAM1表达上调。PRBC在脑微血管中的扣押是脑疟的致病机制之一,ICAM1与PRBC表面的PfEMP1分子的相互作用是扣押的重要的分子基础。ICAM1与CD36在介导粘附时有协同作用。本文综述了近几年ICAM1介导粘附的机制及PRBC内皮细胞之间相互作用的研究进展。     

Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression and function on cultured human glomerular epithelial cells.

Glomerular epithelial cells are involved in extracapillary inflammation (crescents) but the mechanisms of this extracapillary accumulation of macrophages, epithelial cells and occasional lymphocytes are unknown. Human glomerular parietal epithelial cells express ICAM-1 and VCAM-1 on immunohistological stains of renal biopsies. We studied the expression of these cell adhesion molecules on cultured human glomerular epithelial cells (HGEC), their regulation by pro-inflammatory cytokines, and their role in mediating the adhesion of concanavalin A (Con A)-activated peripheral blood mononuclear cells. Human glomerular epithelial cells in culture constitutively express ICAM-1 and VCAM-1. The expression of ICAM-1 was not significantly altered by tumour necrosis factor-alpha (TNF-alpha) (P = 0.32), IL-1 beta (P = 0.24), interferon-gamma (IFN-gamma) (P = 0.66) or IL-4 (P = 0.85). VCAM-1 expression was increased by all four cytokines, but only significantly so by IL-4 (P = 0.0001). Con A-stimulated, monocyte-depleted peripheral blood lymphocytes bound to human glomerular epithelial cells, median 28.9% (range 14.5-37.9%). This adherence was significantly inhibited by anti-ICAM-1 (P = 0.03) and anti-LFA-1 (P = 0.02), but not by anti-VCAM-1 (P = 0.13) or by antibody to von Willebrand factor (P = NS). The interaction between ICAM-1 on HGEC and LFA-1 on mononuclear cells may be important in the pathogenesis of extracapillary inflammation in glomerulonephritis.     

氯沙坦对实验兔颈动脉粥样硬化和血清ICAM-1、VCAM-1的影响

目的:观察氯沙坦对动脉粥样硬化程度和黏附分子的影响.方法:将24只雌雄各半新西兰白兔随机均分为对照组、高脂组、治疗组.对照组喂普通饲料,高脂组喂以高脂饲料,治疗组为高脂饲料加用氯沙坦25mg/(kg·d).分别于实验开始前、开始后第4、8、12周清晨空腹取各组实验动物耳中央静脉血0.5ml,分别测定并比较各组空腹状态下...     

Circulating intercellular adhesion molecule-1 (ICAM-1) as an early and sensitive marker for virus-induced T cell activation

The effect of systemic virus infection on the level of circulating ICAM-1 (cICAM-1) in serum, and the role of virus-activated T cells in this context, were studied using the murine lymphocytic choriomeningitis virus infection as primary model system. A marked virus-induced elevation in cICAM-1 in serum was revealed, the presence of which coincided with the phase of virus-induced T cell activation. However, high levels of cICAM-1 in serum were observed well before maximal T cell activation could be demonstrated. No increase in cICAM-1 was observed in the serum of infected T cell-deficient nude mice, clearly demonstrating that T cells were mandatory. Analysis of MHC class I and MHC class II-deficient mice revealed that either CD4⁺ or CDS⁺ T cells alone are sufficient, despite a markedly reduced inflammatory exudate in the former animals. These results indicate that virus-activated T cells induce shedding of ICAM-1 into the circulation, and this parameter may be used as an early and sensitive marker for immune activation.     

Induction of intercellular adhesion molecule-1 (CD54) on human hepatoma cell line HepG2: influence of cytokines and hepatitis B virus-DNA transfection.

Human hepatocyte expression of intercellular adhesion molecule-1 (ICAM-1) (CD54) was studied in vitro by exposing the well differentiated human hepatoblastoma cell line HepG2 to various cytokines. In addition, hepatitis B virus (HBV)-DNA transfected HepG2 cells were also analysed. Expression of ICAM-1 on HepG2 cells was then revealed with an immunohistochemical procedure. Untreated HepG2 cells were unreactive, but showed strong cytoplasmic ICAM-1 immunoreactivity after treatment with interferon-gamma (IFN-gamma). This induction was completely inhibited by addition of a neutralizing antibody directed to IFN-gamma. IL-1, IL-6, tumour necrosis factor-alpha (TNF-alpha) and IFN-alpha, used alone or in combination, did not induce ICAM-1 expression, neither did they inhibit the IFN-gamma-induced expression of this adhesion molecule on HepG2 cells. Untreated hepatitis B virus-DNA transfected HepG2 cells expressed membranous ICAM-1. These results indicate that IFN-gamma is the main cytokine trigger for ICAM-1 expression on HepG2 cells, suggesting that in areas of liver inflammation this adhesion molecule is up-regulated on hepatocytes by locally released IFN-gamma. In addition, expression of ICAM-1 by hepatitis B virus-DNA transfected HepG2 cells suggests other, still unknown, triggering mechanisms in the induction of such adhesion molecules, for instance gene activation by viral genome, or autocrine virus-induced hepatocellular cytokine production.     

GnRHa长方案促超排卵对种植窗ICAM-I表达的影响及其机制的探讨

目的研究Decapty1/HMG/HCG长方案促超排卵对子宫内膜ICAM-1表达的影响,分析ICAM-1变化与血清E2、P水平之间的相关性,探讨该方案高获卵率而低妊娠率的原因,为临床改善促排卵方案,提高IVF-ET的妊娠率提供理论依据。方法将小白鼠分为NC组和COH组,用免疫组化SP法观察两组小鼠pd1~pd6子宫内膜ICAM-1蛋白的表达。用罗氏电化学发光法检测两组小鼠pd1~pd6血清E2、P的水平。结果NC组中ICAM-1于pd4表达最明显(P(0.01),COH组中ICAM-1于pd3表达最明显(P(0.01)。ICAM-1蛋白的表达高峰和血清高峰点P/E2呈正相关关系(r=0.756,P(0.01)。结论Decapty1/HMG/HCG可能通过改变血清E2、P水平,使子宫内膜种植窗开放异常,导致子宫内膜发育与胚胎发育不同步,降低子宫内膜接受性,这可能是影响IVF-ET妊娠率的重要原因。