烟草烟雾对大鼠脑血管内皮细胞细胞间黏附分子-1表达及脑梗死体积的影响

目的　研究烟草烟雾对大鼠脑血管内皮细胞超微结构 ,细胞间黏附分子 1(ICAM 1)mRNA、ICAM 1表达及大脑中动脉梗死体积的影响。方法　建立大鼠吸烟模型 ,原位杂交及免疫组化检测大鼠脑血管内皮细胞ICAM 1mRNA、ICAM 1的表达 ;建立大鼠左侧大脑中动脉梗死模型 ,测定梗死灶体积占同侧大脑半球体积百分比 ;电镜观察内皮细胞超微结构的改变。结果　 (1)吸烟大鼠脑血管内皮细胞ICAM 1mRNA、ICAM 1表达增加 ,脑梗死灶体积增加 (长期大量吸烟组为4 3 7%± 3 7% ,对照组为 2 7 9%± 1 5 % ,P <0 0 5 ) ;内皮细胞超微结构改变显著。 (2 )戒烟大鼠脑血管内皮细胞ICAM 1mRNA、ICAM 1表达及脑梗死灶体积减小 ,内皮细胞超微结构病理改变明显恢复。结论　烟草烟雾使大鼠脑血管内皮细胞ICAM 1mRNA、ICAM 1表达及大鼠脑梗死灶体积增加 ,二者间存在剂量 效应关系。     

急性期脑梗死患者中性粒细胞与缺氧／复氧内皮细胞粘附性的研究

目的:探讨急性期脑梗死患者外周血PMN与缺氧/复氧(H/R)血管内皮细胞粘附性,以及抗ICAM-1单抗对其的影响。方法:培养的人类脐静脉内皮细胞株ECV-304经(或不经)H/R和抗ICAM-1单抗处理后,分别加入脑梗死患者PMN并检测粘附率。结果:①ECV-304经H/R处理后与脑梗死患者PMN粘附率明显增高;②抗ICAM-1单抗可显著抑制脑梗死患者PMN与H/R ECV-304粘附。结论:①脑梗死患者PMN活化,H/R使血管内皮细胞与PMN粘附性进一步增强;②ICAM-1参与介导脑梗死后PMN与血管内皮细胞粘附,抗ICAM-1单抗可起部分阻断作用。     

脑梗死与血清IL-1β、sICAM-1关系的研究

目的　了解脑梗死患者血清IL - 1β、sICAM - 1含量在急性期和恢复期的变化及意义。 方法　运用酶联免疫吸附法 (ELISA)测定血清中IL - 1β、sICAM - 1含量。 结果　急性期、恢复期脑梗死患者血清IL - 1β、sICAM - 1水平均较对照组显著增高 (P <0 .0 1,P <0 .0 1;P <0 .0 1,P <0 .0 5 ) ,急性期又较恢复期明显增高 (P <0 .0 1,P <0 .0 5 ) ,两者增高程度与梗死灶大小密切相关 ;且急性期脑梗死患者sICAM - 1的水平与IL - 1β的水平呈正相关 (r =0 .6 9,P <0 .0 0 1) ,恢复期脑梗死患者的sICAM - 1与IL - 1β呈正相关 (r =0 .48,P <0 .0 1)。结论　IL - 1β、ICAM - 1可能参与了脑梗死早期的炎症反应及再灌注损伤 ,临床脑梗死I CAM - 1表达上调可能与炎性细胞因子IL - 1β有关     

脑梗死患者颈动脉斑块与炎性因子的相关性研究

目的探讨炎性因子在颈动脉斑块(CAS)脑梗死患者中的动态变化。方法在急性脑梗死(ACI)患者中根据颈部血管彩超结果分为无斑块组42例,稳定斑块组58例,不稳定斑块组64例,观察在脑梗死急性期(2d)及恢复期(15d)血清中IL-18、ICAM1、MMP-9、Lp-PLA、hsCRP水平变化。结果脑梗死急性期无CAS组、稳定CAS组、不稳定CAS组中血清hsCRP、IL-18、ICAM1、MMP-9、Lp-PLA2水平依次升高,组间比较差异有统计学意义(P0.05),恢复期不稳定斑块组的各炎性因子水平仍高于其他2组(P0.05),无斑块组、稳定斑块组中ICAM1、MMP-9血清水平组间比较差异无统计学意义(P0.05)。结论 hsCRP、IL-18、ICAM1、MMP-9、Lp-PLA2与颈动脉粥样斑稳定性有明显相关性,同时在脑梗死急性期炎性因子hsCRP、IL-18、Lp-PLA2可能参与的炎性作用较ICAM1、MMP-9更为明显。     

脑梗死患者血细胞间黏附分子、血小板P选择素的改变

目的　观察脑梗死患者血中性粒细胞表面细胞间黏附分子 (CD5 4 )、血小板P选择素 (CD6 2p)的变化及其临床意义。方法　用流式细胞仪测定 5 0例脑梗死患者和 2 0例健康人血中CD5 4、CD6 2p的表达水平。结果　脑梗死组CD5 4的阳性表达率为 (18 34± 8 6 5 ) % ,CD6 2p的阳性表达率为 (6 15± 3 12 ) % ,均显著高于正常对照组 (P <0 0 1) ,伴高血压脑梗死患者的二项指标分别为 (17 5 2± 7 6 8) %和 (10 16± 4 2 7) % ,均显著高于不伴高血压组和正常组 (P <0 0 5 ) ;CD6 2p与收缩压呈显著直线正相关 (r=0 716 ,P <0 0 5 )。结论　脑缺血后CD6 2p、CD5 4表达明显增高 ,但二者之间无相关性 ,提示脑缺血时两种黏附分子有不同的作用机制 ;CD6 2p与收缩压正相关 (P <0 0 5 ) ,高血压与血小板的活化有关。     

地塞米松对新生大鼠缺氧缺血性脑病脑组织细胞间黏附分子-1表达与白细胞浸润的影响

目的　研究地塞米松预处理对新生大鼠缺氧缺血性脑损伤时脑组织细胞间黏附分子 1(ICAM 1)的表达与白细胞浸润的影响。方法　将 4 8只新生大鼠制作成缺氧缺血性脑病 (HIE)模型 ,于制作模型前 2 4小时即分别予地塞米松预处理组和对照组大鼠腹腔内注射地塞米松 0 1mg/kg、生理盐水 10ml/kg。模型后2 4小时处死大鼠 ,分别进行脑组织ICAM 1免疫组织化学检测、白细胞计数及组织HE染色。结果　ICAM 1平均吸光度 :预处理组 (3 6 2± 1 2 1) ,对照组 (9 4 2± 2 6 5 ) (P <0 0 5 ) ;神经细胞损伤评分 :预处理组 (0 38±0 13) ,对照组 (1 6 3± 0 74 ) (P <0 0 0 1) ;白细胞浸润 :预处理组 (8 4± 1 7) ,对照组 (16 3± 4 6 ) (P <0 0 0 1)。结论　地塞米松预处理能减少HIE时脑组织的ICAM 1蛋白表达及白细胞浸润 ,能减轻脑组织损害程度     

急性缺血性脑血管病患者血ICAM-1、VCAM-1、CD62p的改变及其临床意义

目的　探讨急性缺血性脑血管病患者血中性粒细胞表面细胞间粘附分子 (ICAM- 1)、血管细胞粘附分子 (VCAM- 1)和血小板上 P选择素 (CD6 2 p)的改变及其临床意义。方法　应用流式细胞术测定 12 1例脑缺血患者发病 48小时内 ICAM- 1、VCAM- 1、CD6 2 p的改变。结果　 (1)各种急性脑缺血患者 ICAM- 1均较对照组升高 ,P <0 .0 1;脑血栓形成和腔隙性脑梗死 CD6 2 p升高 ,P <0 .0 5 ;脑血栓形成 VCAM- 1升高 ,P <0 .0 5。 (2 )脑梗死面积≥ 1.5 cm2 者 ICAM- 1、CD6 2 p较 <1.5 cm2 者高。 (3) ICAM - 1与收缩压呈正相关。结论　 3种粘附分子在不同脑缺血患者发病初表达不同 ,测定 ICAM - 1和 CD6 2 p有助于脑缺血病情观察     

低强度氦氖激光对内皮细胞增殖与ICAM-1的影响

目的 研究低强度氮氖激光对内皮细胞增殖与内皮细胞间黏附分子(Intercellular Adhe-sio Molecule-1,ICAM一1)表达的影响。方法 应用不同功率低强度氮氖激光辐照体外培养的血管内皮细胞，采用噻唑蓝(MTT)比色法研究内皮细胞的增殖情况，用免疫组化方法观测其ICAM一1的变化。结果 在辐照后48小时、72小时、96小时发现，随着辐照次数与辐照时间的延长，反映内皮细胞增殖的光密度(OD)值逐渐变高，其增高无统计学意义(P＜0．05)；内皮细胞ICAM一1表达则逐渐减低。结论 经低强度氮氖激光辐照后，内皮细胞没有出现增殖，但能抑制内皮细胞ICAM一1表达。     

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、     

大鼠脑缺血再灌注模型ICAM-1表达与白细胞浸润关系及亚低温干预治疗的研究

目的　研究大鼠局灶性脑缺血再灌注后不同时程脑组织中的细胞间粘附分子 1 (ICAM 1 )表达规律 ,及其与白细胞浸润的关系 ,并探讨亚低温的治疗作用。方法　采用大鼠大脑中动脉 (MCA)线拴闭塞 /再通法建立大鼠局灶性脑缺血 再灌注模型 ,常温组分别于脑缺血 3小时再灌注 2小时、8小时、2 4小时、48小时、72小时后断头取脑 ;假手术组及亚低温组于脑缺血 3小时再灌注 2 4小时断头取脑 ,行ICAM 1免疫组化及组织HE染色 ,测定ICAM 1表达阳性微血管数及白细胞计数。结果　⑴脑缺血再灌注后 2小时 ,脑缺血的坏死周边区的微血管内皮细胞表达ICAM 1出现增高趋势 ,并于 2 4小时达到高峰 ,各组之间及各组与假手术组间均有显著差异 (均P <0 0 5) ;⑵脑缺血再灌注 8小时出现白细胞浸润 ,且浸润高峰也在 2 4小时 (P <0 0 1 ) ;⑶ICAM 1的表达与白细胞浸润呈正相关 (r =0 .82 7,P <0 0 1 ) ;⑷缺血早期进行亚低温治疗能明显减轻缺血再灌注后ICAM 1的表达及减少白细胞浸润 (P <0 0 1 )。结论　脑缺血再灌注后ICAM 1可介导白细胞和内皮细胞的粘附 ,加速白细胞的浸润 ,提示ICAM 1是造成脑缺血损伤的重要因素之一 ;亚低温的干预治疗能明显减轻缺血再灌注后脑组织病理形态学的损害程度。     

脑缺血抗细胞间粘附分子—1抗体作用的实验研究

目的探讨抗细胞间粘附分子－１（ＩＣＡＭ－１）抗体保护神经元缺血性损伤的作用机制。方法分离培养鼠脑毛细血管内皮细胞（ＣＣＥＣ）和多形核白细胞（ＰＭＮ），利用微管吸吮技术，观察ＰＭＮ与ＣＣＥＣ间粘附力学特性的变化。结果脑缺血－再灌注后各时间点，ＰＭＮ与ＣＣＥＣ的粘附力和粘附应力均明显高于正常对照组和伪手术组（Ｐ＜０．０１）；加抗ＩＣＡＭ－１抗体后，细胞粘附力和粘附应力均明显下降（Ｐ＜０．０５或Ｐ＜０．０１）。结论脑缺血－再灌注损伤后抗ＩＣＡＭ－１抗体使ＰＭＮ与ＣＣＥＣ粘附力减小，粘附应力下降；抗粘附分子抗体将可能成为治疗缺血性脑血管疾病的一条新的有效途径     

Expression of P-selectin and intercellular adhesion molecule-1 in human brain after focal infarction or cardiac arrest

Data from experimental studies indicate that acute inflammation contributes to ischaemic brain damage. Tethering of neutrophils to brain endothelium is mediated by selectins, and subsequent adhesion and migration by endothelial intercellular adhesion molecule-1 (ICAM-1) and neutrophil CD18. In experimental studies of ischaemia-reperfusion injury, brain damage has been ameliorated by administration of antibodies to these adhesion molecules. We studied the expression of P-selectin and ICAM-1 in sections of brain from patients who had experienced cardiac arrest or focal brain infarction, and who died 3.5 h to 9 days later. Endothelial immunopositivity for both adhesion molecules was maximal at about 2-3 days then declined. Between 1 day and 3 days, P-selectin was also detected on platelets in blood vessels within infarcted tissue. Within infarcts, but not sections of brain from cardiac arrest patients, P-selectin and ICAM-1 were again detectable at 1 week, when hyperplastic endothelial cells were labelled in capillaries in and immediately adjacent to the infarcted tissue. The finding that P-selectin and ICAM-1 are upregulated within focally infarcted brain tissue supports the concept that blocking neutrophil adhesion may be of benefit in treating atherothrombotic strokes in man.     

Upregulation of intercellular adhesion molecule-1 expression on human endothelial cells by tumour necrosis factor-alpha in an in vitro model of the blood-brain barrier.

Adhesion molecules on the endothelial surface of the blood-brain barrier (BBB) play an important role in the pathogenesis of many encephalopathies, including multiple sclerosis (MS) and cerebral malaria (CM). The expression of four surface molecules of relevance to MS and CM on the immortalized human umbilical vein endothelial cell line, ECV304, was investigated using immunofluorescence flow cytometry. We found that ECV304 cells express intercellular adhesion molecule-1 (ICAM-1) and low levels of CD36, but not vascular cell adhesion molecule-1 (VCAM-1) or E-selectin. This expression pattern was unaltered on ECV304 cells which were co-cultured with C6 glioma cells; conditions under which the endothelial cells display enhanced barrier formation. Tumour necrosis factor-alpha (TNF-alpha), which is elevated in MS and CM, decreased the integrity of the barrier in co-cultured endothelial cells and upregulated the expression of ICAM-1 nine-fold. The significance of elevated ICAM-1 expression in relation to the binding of parasitised erythrocytes at the BBB in CM is discussed.     

急性脑梗死患者中性粒细胞粘附分子表达的变化及意义探讨

目的探讨急性脑梗死(cerebral infarction,CI)患者中性粒细胞(polymorphonuclear neutrophil,PMN)表面粘附分子CD62L和CD11b/CD18表达及其意义。方法选择急性血栓形成性脑梗死患者40例,年龄、性别等与之匹配的健康志愿者30例作为对照。运用流式细胞仪对所有对象检测外周血中PMN表面粘附分子CD62L和CD11b/CD18表达。结果相对于正常组粘附分子CD62L平均抗体阳性表达率(73.316±1.276)%,CI组(61.058±8.925)%显著降低(P<0.001);相对于正常组CD11b/CD18平均阳性表达率(20.031±0.540)%,CI组(55,598±0.540)%显著升高。CI组内部CD62L、CD11b/CD18相关分析,二者呈明显负相关,相关系数为r=-0.259(P<0.001)。结论在急性血栓形成性脑梗死的急性期,PMN处于活化状态,表现为粘附分子CD62L表达的下调和CD11b/CD18表达的上调。以细胞粘附为表现的PMN活化加快了血栓的进程,可能是血栓形成的重要发病原因之一。     

Assembly of high molecular weight kininogen and activation of prekallikrein on cell matrix

Investigations determined if extracellular matrix of endothelial cells (EC) is a platform for HK assembly and PK activation. In buffers containing bovine serum albumin, biotin-HK binding to ECV304 cells or their matrix requires > or = 50 microM added Zn2+. Ortho-phenanthroline or a HK domain 5 peptide blocks HK binding. Binding to umbilical vein EC or matrix, but not ECV304 cells or matrix, is mediated by cytokeratin 1. Biotin-HK binds to ECV304 cells or matrix with a Kd of 15.8 or 9.0 nM and a Bmax of 2.6 x 10(7) or 2.4 x 10(7) sites/cell, respectively. PK activation on ECV304 cells or matrix is blocked by antipain or SBTI and corn trypsin inhibitor partially inhibits kallikrein formation. PK activation occurs on ECV304 cells or matrix prepared without serum or in human factor XII deficient serum, indicating that the PK activator is not factor XIIa. EC matrix promotes plasminogen activation after the assembly of HK, PK and pro-urokinase. These studies indicate that matrix of various EC has the ability to assemble HK allowing for PK activation and subsequent activities.     

Upregulation of intercellular adhesion molecule-1 expression on human endothelial cells by tumour necrosis factor-α in an in vitro model of the blood–brain barrier

Adhesion molecules on the endothelial surface of the blood–brain barrier (BBB) play an important role in the pathogenesis of many encephalopathies, including multiple sclerosis (MS) and cerebral malaria (CM). The expression of four surface molecules of relevance to MS and CM on the immortalized human umbilical vein endothelial cell line, ECV304, was investigated using immunofluorescence flow cytometry. We found that ECV304 cells express intercellular adhesion molecule-1 (ICAM-1) and low levels of CD36, but not vascular cell adhesion molecule-1 (VCAM-1) or E-selectin. This expression pattern was unaltered on ECV304 cells which were co-cultured with C6 glioma cells; conditions under which the endothelial cells display enhanced barrier formation. Tumour necrosis factor-α (TNF-α), which is elevated in MS and CM, decreased the integrity of the barrier in co-cultured endothelial cells and upregulated the expression of ICAM-1 nine-fold. The significance of elevated ICAM-1 expression in relation to the binding of parasitised erythrocytes at the BBB in CM is discussed.     

缺氧复氧对血管内皮细胞ICAM-1表达及内皮-白细胞粘附的影响

目的：评价缺氧／复氧后血管内皮细胞ＩＣＡＭ－１表达及内皮－白细胞粘附率的变化。方法：体外培养大鼠骨髓血窦内皮细胞,缺氧９０ｍｉｎ,分别给予复氧１ｈ,２ｈ,４ｈ,８ｈ,１２ｈ,２４ｈ,用半定量ＥＬＩＳＡ法测ＩＣＡＭ－１的表达量,同时人皮细胞对中性粒细胞的粘附率。     

急性脑血管病患者血清P-选择素的含量变化及其临床意义

目的探讨P-选择素(Ps)在脑梗死发生、发展中的作用。方法采用ELISA测定54例脑梗死患者、15例脑出血患者、20例正常对照血清Ps含量。结果脑梗死组发病3d内血清Ps水平明显高于脑出血组及对照组,后两组无显著差异;脑梗死组发病3d内血清Ps水平与发病后1周无显著差异,但均明显高于发病后2周,发病后2周与对照组无显著差异;脑梗死组发病3d内血清Ps水平与梗死灶体积呈正相关。结论Ps参与脑缺血再灌注损伤,可作为脑梗死早期诊断及鉴别诊断的依据,干预其产生和作用途径可改善脑梗死的预后。     

脑梗死患者急性期可溶性粘附分子的变化及临床意义

目的:为了解脑梗死患者急性期可溶性粘附分子的变化及临床意义。方法:采用双抗体夹心ELIsA法测定76例脑梗死患者血清sICAM-1、sVCAM-1、sE-selectine,并与52例TIA患者和40例健康老年人对照比较。结果:脑梗死患者24小时内血清sICAM-1、sVCAM-1、sE-selectine水平明显高于TIA和健康对照组(P<0.01)。大梗死灶组血清sICAM-1、sVCAM-1、sE-selectine水平明显高于中梗死灶组和小梗死灶组。脑梗死患者血清sICAM-1、sVCAM-1、sE-selectine水平在脑梗死发生24小时至7天呈现上升趋势,7天至14天呈下降趋势。结论:sICAM-1、sVCAM-1、sEselectine与急性脑梗死密切相关,参与了缺血后脑组织损伤的病理过程。在脑梗死急性期阻断粘附分子的表达可能有助于减轻缺血性脑损伤。