可溶性细胞间黏附分子-1、血管细胞黏附分子-1与急性脑梗死关系的研究

急性脑梗死(acute cerebral infarction,ACI)后会引发颅内炎性反应。研究显示,缺血区内大量白细胞(WBC)黏附于血管内皮细胞表面并外渗。炎性介质细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)与这一过程密切相关,而外周血可溶性ICAM-1(sICAM-1)、VCAM-1(sVCAM-1)主要来源于细胞表面模型ICAM-1、VCAM-1,其血浆水平的增高是内皮细胞和WBC损害或激活的标志。作者观察了38例ACI、33例恢复期脑梗死(remissonstages cerebral infarction,RSCI)患者血浆sICAM-1、     

脑出血患者血清细胞间黏附分子-1与血管细胞黏附分子-1含量变化

目的观察脑出血患者1d、3d、7d、14d血清中可溶性细胞间黏附分子-1(sICAM-1)、可溶性血管细胞黏附分子-1(sV-CAM-1)含量变化,探讨临床意义。方法采用双抗夹心酶联免疫吸附法(ELISA)测定血清中sICAM-1、sVCAM-1含量。结果脑出血患者sICAM-1、sVCAM-1含量第1d开始升高,与对照组比较差异无统计学意义(P>0.05);第3d、7d含量显著升高,与对照组相比差异有统计学意义(P<0.01);第14d含量开始下降,与对照组相比差异有统计学意义(P<0.01);重型脑出血组与轻型脑出血组比较,第3d、7d差异均有统计学意义(P<0.05,P<0.01)。结论ICAM-1、VCAM-1参与脑血肿周围脑组织炎症反应及继发性脑组织损伤。     

内皮微粒在肾移植急性排斥反应中的诊断作用

背景：血管内皮细胞的变化与移植排斥反应的关系极为密切,内皮微粒脱落于激活或凋亡的内皮细胞,能直接而特异地反映血管内皮细胞的变化,检测血浆中内皮微粒对肾移植排斥反应的诊断监测具有一定的理论和实际意义。目的：探讨肾移植急性排斥反应时循环内皮微粒的数量和表型的变化及与急性排斥反应之间的关系。方法：建立同基因和同种异基因大鼠腹腔原位肾移植模型;移植后5 d苏木精-伊红染色观察肾组织的病理学改变,并进行Banff评分;采用免疫组化法检测肾组织中细胞间黏附分子1表达;采用流式细胞术检测血浆中CD144+内皮微粒数量及细胞间黏附分子1+/CD144+内皮微粒的数量;分析内皮微粒的数量和表型与肾组织病理变化的关系。结果与结论：与同基因移植组比较,异基因移植组Bnaff评分明显增加(P < 0.01),肾组织中细胞间黏附分子1表达明显增强(P < 0.01);与同基因移植组比较,异基因移植组CD144+内皮微粒的数量和携带细胞间黏附分子1的内皮微粒的水平明显增加(P < 0.01)。内皮微粒的数量与移植肾急性排斥反应的程度呈正相关(P < 0.01),携带细胞间黏附分子1内皮微粒的水平与移植肾脏中细胞间黏附分子1的表达呈正相关(P < 0.01)。提示肾移植后对内皮微粒数量和表型进行检测对诊断急性排斥反应的发生有一定意义。     

大鼠骨髓间充质干细胞血管细胞黏附分子1及细胞间黏附分子1的表达

背景：骨髓间充质干细胞系统性输注后,何种因素促使其迁移到正确部位尤为关键,目前认为黏附分子在介导骨髓间充质干细胞向缺血或损伤组织迁移过程中起重要作用。 目的：观察血管细胞黏附分子1与细胞间黏附分子1在大鼠骨髓间充质干细胞中的表达。 方法：采用直接贴壁法体外分离培养大鼠骨髓间充质干细胞,免疫细胞化学染色检测血管细胞黏附分子1及细胞间黏附分子1蛋白的表达,应用免疫荧光直标法在流式细胞仪上检测血管细胞黏附分子1及细胞间黏附分子1抗原的表达率,RT-PCR半定量分析血管细胞黏附分子1及细胞间黏附分子1 mRNA的表达。 结果与结论：免疫细胞化学染色结果显示,骨髓间充质干细胞血管细胞黏附分子1呈弱阳性表达,细胞间黏附分子1呈强阳性表达。流式细胞仪检测结果显示,血管细胞黏附分子1表达率为6%,细胞间黏附分子1表达率为100%。RT-PCR检测结果显示,血管细胞黏附分子1 mRNA呈微弱表达,细胞间黏附分子1 mRNA呈高度表达。提示在生理状态下,体外培养的大鼠骨髓间充质干细胞低表达血管细胞黏附分子1,高表达细胞间黏附分子1。     

脑出血患者血清可溶性细胞间黏附分子-1浓度的动态变化及其意义

目的　研究脑出血患者血清可溶性细胞间黏附分子 1(sICAM 1)浓度的动态变化及其意义。方法　采用酶联免疫吸附法 (ELISA)检测 5 0例脑出血患者发病后不同时间血清sICAM 1的含量 ,并与正常人比较 ,及出血量 >2 0ml与≤ 2 0ml患者的血清sICAM 1浓度比较。结果　脑出血组急性期不同时点血清sICAM 1浓度均明显高于对照组 (均P <0 0 0 1)。脑出血组血清sICAM 1浓度于发病后 2 4h升高 ,3～ 7d达高峰 ,病后14d明显下降 ,但仍明显高于对照组。出血量 >2 0ml患者血清sICAM 1浓度明显高于出血量≤ 2 0ml患者(P <0 .0 1～ 0 0 0 1)。结论　sICAM 1参与了脑出血的发生和发展过程 ;观察血清sICAM 1浓度 ,对判断病情及出血量有一定的帮助。     

脑缺血再灌注大鼠细胞间黏附分子-1、血管细胞间黏附分子-1的表达及β-七叶皂甙钠的干预作用

目的研究局灶性脑缺血再灌注过程中脑缺血区细胞间黏附分子-1(ICAM-1)、血管细胞间黏附分子-1(VCAM-1)的表达规律,并探讨β-七叶皂甙钠对其干预的脑保护作用。方法采用线栓法建立大鼠脑缺血再灌注模型,同时应用β-七叶皂甙钠予以干预。用HE染色和免疫组化染色观察大鼠脑缺血后再灌注不同时点组织学改变和ICAM-1、VCAM-1的阳性表达。结果(1)β-七叶皂甙钠明显减轻缺血再灌注后的脑组织损伤;(2)脑缺血再灌注后缺血区微血管内皮细胞ICAM-1、VCAM-1表达增加,ICAM-1于再灌注后24h表达达高峰,VCAM-1.于再灌注后24～48h表达达高峰,随后降低,但再灌注后72h两者表达仍高于正常水平;(3)β-七叶皂甙钠可以显著降低脑缺血再灌注后24h、48h缺血区ICAM-1、VCAM-1的表达。结论脑缺血再灌注后ICAM-1、VCAM—1大量表达,可能是脑缺血再灌注损伤的机制之一;β-七叶皂甙钠能降低ICAM-1和VCAM-1的表达及减轻脑组织损伤,有脑保护作用。     

脑缺血时干扰素-γ与细胞间黏附分子-1表达的相关性研究

该研究就脑缺血时干扰素-γ（IFN-γ）与细胞间黏附分子-1（ICAM-1）表达是否相关，即脑缺血时IFN-γ是否也是影响ICAM-1表达的一个因素进行了探讨。     

细胞间黏附分子-1启动子甲基化水平与脑梗死的相关性

目的 评估细胞间黏附分子-1(Intercellular adhesion molecule-1,ICAM-1)基因启动子区甲基化水平与脑梗死的相关性。方法 对2017年9月-2018年9月于解放军第960医院就诊患者进行回顾性分析,根据诊断标准挑选152例脑梗死患者为病例组,同期于该院体检健康者 152 例为对照组,采用酶联免疫吸附法(Enzyme linked immunosorbent assay,ELISA)检测2组受试者外周血ICAM-1水平,使用荧光定量甲基化特异性聚合酶链反应(Quantitative Methylation Specific PCR,qMSP)法测定2组受试者ICAM-1甲基化程度。结果 病例组外周血ICAM-1水平显著高于对照组(T=20.27,P<0.001); 病例组ICAM-1基因甲基化程度显著低于对照组(Z=-3.158,P=0.002); 病例组亚组分析发现有吸烟史者甲基化程度更低(Z=-3.305,P=0.001); 2组ICAM-1甲基化程度均与ICAM-1水平呈显著负相关(病例组r=-0.756,P<0.001; 对照组r=-0.823,P<0.001)。结论 ICAM-1低甲基化通过促进ICAM-1的高表达,参与脑梗死的病理过程,可能通过调节基因表达水平来影响脑梗死的患病风险。ICAM-1启动子区甲基化程度升高可作为脑梗死的保护因素。     

微创血肿清除术对脑出血患者血浆细胞间黏附分子-1的影响

目的探讨高血压性脑出血微创术对清除血肿后脑水肿患者血浆细胞间黏附分子-1（ICAM-1）的影响。方法113例脑出血患者随机分为内科治疗组60例、微创术血肿抽吸引流组53例;采用酶联免疫法（ELISA）测定脑出血后治疗前、治疗后第3天、第7天和第14天血浆ICAM。1含量。结果微创组和内科治疗组血清ICAM-1含量均升高;两组治疗后第3、7天的含量与治疗前（发病24h内）比较,差异有统计学意义（P〈0．05）;两组治疗后不同时间点血清ICAM-1含量比较,差异有统计学意义（P〈0．05）。结论微创术能降低血清ICAM-1水平。     

肺移植前后可溶性细胞间黏附分子1的变化

背景：应用生物素-链亲和素系统建立的可溶性细胞间黏附分子1测定法,是一种敏感度高、可测范围广的检测方法。 目的：建立可溶性细胞间黏附分子1生物素-链亲和素系统时间分辨荧光免疫分析方法并应用于临床,探讨肺移植前后血清可溶性细胞间黏附分子1的变化及临床意义。 方法：使用2株匹配的单克隆抗体分别作为捕获抗体和检测抗体,利用制备的铕标记链亲和素(SA-Eu3+)作为示踪物并与生物素化的检测抗体特异结合,建立双位点多层夹心法,通过对30例健康人血清可溶性细胞间黏附分子1检测和26例肺移植受者手术前后血清可溶性细胞间黏附分子1的变化测定,对可溶性细胞间黏附分子1生物素-链亲和素系统方法学和在肺移植术前后的临床应用价值进行评价。 结果与结论：30例健康对照测定结果为(348.63±69.12) µg/L。移植前可溶性细胞间黏附分子1与对照组无显著性差别;移植后,各组与对照组之间比较差异有显著性意义(P < 0.05),急性排斥反应时血清可溶性细胞间黏附分子1升高,并发感染时降低,但各组之间比较无明显差别。表明可溶性细胞间黏附分子1生物素-链亲和素系统是一种新型的高灵敏度、宽范围的非放射性标记免疫分析法,对肺移植受者移植前后监测血清可溶性细胞间黏附分子1可作为辅助诊断急性排斥反应的免疫学指标。     

Interleukin-6 and soluble intercellular adhesion molecule-1 in acute brain ischaemia

Inflammation plays a critical role in the pathogenesis of atherothrombosis. Our aim was to examine the association between plasma concentrations of inflammatory biomarkers and severity and outcome of acute brain ischaemia. Plasma samples were collected within 36 h of symptom onset in patients with acute brain ischaemia, and assessed by conventional ELISA kits for concentration of interleukin-6 (IL-6) and soluble intercellular adhesion molecule-1 (sICAM-1). Patients were assessed serially for stroke severity (National Institute of Health stroke scale) and outcome during follow-up (modified Rankin Scale, mRS; and Stroke Impact Scale-16, SIS). Patients ( n  = 113, 65% men, mean age 64 ± 12 years) had a mean IL-6 concentrations of 5.1 ± 5.0 pg/ml and sICAM-1 of 377 ± 145 ng/ml. IL-6, but not sICAM-1, concentrations were strongly associated with stroke severity ( P  < 0.01 at all serial assessments). Ln-transformed IL-6 levels (per 1 SD) were associated with disability (mRS ≥2, OR = 1.7; 95% CI 1.1–3.0) and poor physical function (SIS ≤85, OR = 1.7; 95% CI 1.0–2.8). Further adjustment for baseline stroke severity, however, eliminated these associations. Our results suggest that high plasma concentrations of the inflammatory biomarker IL-6 but not sICAM-1 are associated with stroke severity and poorer functional outcome. IL-6 does not add, however, additional prognostic information for stroke outcome beyond that conveyed by the stroke severity.     

Circulating intercellular adhesion molecule-1 and E-selectin in acute ischemic stroke.

Exposure of endothelia to hypoxia followed by reperfusion, results in increased leukocyte activation and extravasation. These leukocytes potentiate ischemic neuronal damage. Extravasation of leukocytes is guided by adhesion molecule interactions on inflammatory and endothelial cells. Circulating adhesion molecules rapidly appear in peripheral blood. Commercially available ELISA kits were used to determine serum levels of E-selectin and intercellular adhesion molecule-1 (ICAM-1) in 36 patients at 1, 3, and 14 days after acute ischemic stroke. E-selectin levels were nonsignificantly increased at day 1, and decreased thereafter, reaching significantly lower values at day 14 in the stroke patients. ICAM-1 levels were similar in stroke patients at each sampling period, and did not differ from those of controls. Our data on ICAM-1 are in line with those of a recently published study. The decreasing circulating E-selectin may stem from endothelial cell damage, alterations in cytokine interactions, or unknown factors.     

Circulating intercellular adhesion molecule-1 levels and neutrophil adhesion in stroke

To examine whether changes in leukocyte adhesion properties occur during stroke, we measured circulating serum intercellular adhesion molecule 1 (cICAM-1) levels and neutrophil adhesion in acute stroke, patients at high risk of stroke, and in matched controls. Levels of cICAM-1 were significantly lower in the stroke group (186.2 ± 15.6 ng ml⁻¹) compared to controls (257.7 ± 24.8) and risks (257.7 ± 16.5). Neutrophil adhesion was significantly higher in the stroke group (23.6 ± 4.3%; n = 14) compared to controls (9.7 ± 2.3%; n = 12) and risks (12.7 ± 2.5%; n = 13). These data suggest that changes in leukocyte adhesion dynamics are occuring in acute stroke.     

Differential expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in chronic murine retroviral encephalitis

The cell adhesion molecules, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1, are important mediators of immune interactions within the central nervous system (CNS). A wide variety of pro-inflammatory insults to the brain, including viral infection, result in upregulation of these molecules on brain endothelial cells, astrocytes, and microglia. This study investigated the expression of ICAM-1 and VCAM-1 in chronic encephalitis induced by infection with a temperature sensitive (ts-1) strain of Moloney murine leukaemia virus (MoMuLV), an ecotropic murine retrovirus. During the late stages of disease, viral antigen was present in both endothelial cells and microglia, but not astrocytes, in regions of spongiform change and gliosis. In these areas, ICAM-1 staining was detected on activated microglia, but not on endothelial cells or astrocytes. In contrast, no cells showed increased VCAM-1 expression in the CNS. These findings demonstrate that there is cell-specific, differential expression of these adhesion molecules in ts-1 retroviral encephalitis. The lack of endothelial cell expression correlates with the characteristic lack of lymphocytic infiltrate in this chronic retroviral encephalitis and suggests that increased microglial ICAM-1 expression may play a role in the pathogenesis of MoMuLV (ts-1)-mediated neurodegeneration.     

Serum levels of soluble intercellular adhesion molecule-1 and soluble endothelial leukocyte adhesion molecule-1 in Alzheimer's disease

Serum soluble intercellular adhesion molecule-1 (s-ICAM-1) and soluble E-selectin (s-ELAM-1) were evaluated in 25 patients with Alzheimer's disease (AD), 54 patients with noninflammatory neurological diseases (NIND), and 15 control subjects. Patients with AD had a higher s-ICAM-1 level compared with the NIND patients and the control subjects (P< .001 and P< .04, respectively). The presence of high s-ICAM-1 values may be related to immunological processes involved in pathogenetic mechanisms of AD. The not statistically significant values of (s-ELAM-1), a glycoprotein considered an exclusive marker of endothelial activation, compared with the NIND patients and healthy subjects (P< .47 and P< .17, respectively), seem to suggest the neural rather than the endothelial s-ICAM origin in patients with AD.     

Serum levels of intercellular adhesion molecule-1 and E-selectin in patients with acute ischaemic stroke

To investigate the role of circulating intercellular adhesion molecule-1 (ICAM-1) and E-selectin in ischaemic stroke, serum levels of ICAM-1 and E-selectin were measured by ELISA in 51 patients with acute ischaemic stroke within 24 h, and in 25 age-matched healthy controls and 10 young healthy volunteers. Carotid Doppler ultrasonography showed a significant stenosis (>50%) of the carotid or vertebrobasilar artery in 11 of 51 stroke patients. Serum levels of ICAM-1 [mean (SE)] were higher (P <0.01) in patients with ischaemic stroke [381 (30) ng/ ml] than in age-matched controls [271 (27) ng/ml] and young controls [246 (6) ng/ml]. There was no significant difference in serum E-selectin levels [mean (SE)] among stroke patients, age-matched and young controls [47 (6), 39 (3), and 41 (3) ng/ ml, respectively; P = NS]. The leucocyte count [mean (SD)] was higher (P < 0.01) in patients with ischaemic stroke [8310 (2800)] than in age-matched controls [6040 (930)]. Serum levels of ICAM-1 and E-selectin did not significantly differ between patients with or without abnormal carotid or vertebrobasilar artery disease. In conclusion, serum ICAM-1 level and leucocyte count were elevated in acute ischaemic stroke within 24 h, while the E-selectin level did not change significantly. This finding suggests that adhesion molecules may play an important role in the post-rolling process of leucocyte-endothelial cell interaction in acute ischaemic stroke. Received: 14 September 1995 Received in revised form: 7 June 1996 Accepted: 26 June 1996     

Involvement of intercellular adhesion molecule-1 in myelin recognition by macrophages

Macrophages play a crucial role in myelin removal during nerve degeneration and demyelination. The exact mechanisms of myelin recognition and uptake are not yet defined. The present experiments aimed at defining the role of intercellular adhesion molecule-1 (ICAM-1) in this process. Myelin phagocytosis was studied in an established in vitro model of cultured macrophages and sciatic nerves. Cocultures of wild-type C57BL macrophages with sciatic nerves resulted in a massive invasion of the nerves by macrophages with subsequent removal of myelin. In contrast, when macrophages of ICAM-1-deficient animals were cocultured with wild-type nerves, myelin phagocytosis was significantly retarded, whereas cell invasion was completely undisturbed. These data indicate that the ICAM-1 molecule acts as a costimulatory signal in myelin recognition and uptake by macrophages. Received: 3 January 2000 / Revised, accepted: 7 February 2000     

Intra-ischemic hypothermia attenuates intercellular adhesion molecule-1 (ICAM-1) and migration of neutrophil

Adhesion of neutrophil to the endothelium and subsequent transmigration has been reported to contribute to progression of focal ischemia. Hypothermia has been known to attenuate ischemic insult through various mechanisms of action. The authors evaluated the effect of hypothermia on expression of intercellular adhesion molecule-1 (ICAM-1) protein and on transmigration of neutrophil with immunohistochemical method. Transient focal ischemia model in rats was employed, and animals received 2 h of either normothermic or hypothermic ischemia. To confirm the effectiveness of hypothermia on neuroprotection, cortical infarct area was compared between the two groups. Our results demonstrated that hypothermia reduced both the number of microvessels expressing ICAM-1 and that of neutrophils migrating into ischemic tissue. Comparison of cortical infarct area showed persistent protective effect. This study indicates that reduction of ICAM-1 expression and subsequent reduction of migrating neutrophil in hypothermia can contribute to attenuation of ischemic damage.