载脂蛋白C3促进THP-1细胞向小鼠主动脉黏附

目的 探讨载脂蛋白C3(APOC3)对THP-1细胞与小鼠主动脉黏附效应的影响.方法 在无菌环境下应用外科显微技术分离C57BL/6小鼠主动脉,在体外给予APOC3刺激16 h后与标记有CFSE荧光的单核细胞来源THP-1细胞黏附1h,观察黏附效应的变化,同时应用免疫组化方法检测血管黏附分子1(VCAM-1)和细胞间黏附分子1(ICAM-1)的表达.结果 给予APOC3刺激的主动脉与对照主动脉相比,与THP-1细胞的黏附效应增加,VCAM-1和ICAM-1表达上调,且前者比后者上调显著.结论 载脂蛋白C3促进THP-1细胞向小鼠主动脉黏附.     

PSMA7对A549细胞表面黏附分子表达的影响

目的探讨PSMA7表达量的变化对A549细胞表面黏附分子ICAM-1,VCAM-1和CD44表达的影响。方法采用流式细胞仪分别检测高表达PSMA7的A549细胞[pcDNA3.1(-)/PSMA7组]和低表达PSMA7的A549细胞(shPSMA7组)表面黏附分子ICAM-1,VCAM-1和CD44的表达情况。结果与高表达阴性对照组[pcDNA3.1(-)组]相比,pcDNA3.1(-)/PSMA7组的ICAM-1(t=86.325,P=0.000)和VCAM-1(t=16.337,P=0.000)的表达量均显著降低,CD44表达量则无明显变化(t=-0.545,P=0.615),而与低表达阴性对照组(shNC组)相比,shPSMA7组ICAM-1(t=-119.827,P=0.000)和VCAM-1(t=-26.68,P=0.000)表达量均显著增高,CD44表达量则无明显变化(t=-848,P=0.444)。与pcDNA3.1(-)组相比,pcDNA3.1(-)/PSMA7组穿膜侵袭细胞的数量明显减少(t=3.553,P=0.024),而shPSMA7组明显高于shNC组(t=-3.207,P=0.033)。结论高表达或干扰PSMA7可影响A549细胞表面黏附分子ICAM-1,VCAM-1的表达,提示PSMA7可能因此参与肺腺癌细胞的侵袭和转移。     

苦瓜蛋白对低剪切应力下apoE~(-/-)小鼠内皮-间充质转化的影响

目的:探讨苦瓜蛋白对低剪切应力内皮-间充质转化的影响,探讨其抗动脉粥样硬化作用新机制。方法:构建apoE~(-/-)小鼠颈动脉低剪切应力模型,将20只apoE~(-/-)小鼠随机分为苦瓜蛋白组和模型组,均予以高脂饮食喂养,苦瓜蛋白组腹腔注射苦瓜蛋白(5 mg·kg~(-1)·d~(-1)),模型组注射等体积的生理盐水。ELISA检测apoE~(-/-)小鼠血浆中炎症因子水平;Western blot和免疫荧光检测颈总动脉中内皮及间充质标志物表达和共定位情况,以及细胞间黏附分子1(ICAM-1)和血管细胞黏附分子1(VCAM-1)表达水平。结果:模型组低剪切应力下内皮完整性受损,且出现了动脉粥样硬化病变和内皮-间充质转化,但均可被苦瓜蛋白可所抑制。与模型组比较,苦瓜蛋白组内皮标志物血管内皮钙黏蛋白(VE-cadherin)表达显著上调(P0.05),间充质标志物α-平滑肌肌动蛋白(α-SMA)表达显著下调(P0.05)。机制研究发现,苦瓜蛋白可降低血清炎症因子肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)及IL-1β水平,以及黏附分子ICAM-1和VCAM-1的表达水平。结论:苦瓜蛋白能减轻低剪切应力下内皮-间充质转化,与其抑制炎症因子和黏附分子的表达有关。     

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。     

IL-35对sCD40L刺激后的人脐静脉血管内皮细胞黏附功能的影响

目的 探讨白细胞介素(IL)-35对可溶性CD40配体(sCD40L)刺激后血管内皮细胞黏附功能的影响。方法 选取2020年1月至12月于滨海县人民医院诊治的30例下肢深静脉血栓急性期患者(DVT组)和30例健康体检者(HC组)。采集外周静脉血，ELISA检测血清IL-35、sCD40L、血管细胞间黏附分子(VCAM-1)、细胞间黏附分子(ICAM-1)、P-选择素和血管性血友病因子(vWF)的水平。体外培养人脐静脉血管内皮细胞(HUVECs),分为对照组、sCD40L组和IL-35组。ELISA检测细胞培养上清液中VCAM-1、ICAM-1、P-选择素和vWF的水平；Western blot检测细胞VCAM-1、ICAM-1、P-选择素和vWF蛋白的表达；免疫荧光法检测血小板和外周血单个核细胞对HUVECs的黏附。结果 DVT组血清中IL-35表达显著低于对照组(P<0.05),sCD40L、VCAM-1、ICAM-1、P-选择素和vWF的表达显著高于对照组(P<0.05)。体外实验表明，IL-35能显著抑制sCD40L刺激后HUVECs VCAM-1、ICAM-1、P-...     

血管内皮生长因子和血小板反应蛋白-1在大鼠胸主动脉瘤中的表达 

目的 探讨血管内皮生长因子（VEGF）及血小板反应蛋白-1（TSP-1）在实验性大鼠胸主动脉瘤中的表达及其意义。方法 30只成年雄性Wistar大鼠随机分为对照组和手术组,每组15只。采用氯化钙（CaClSUB>2/SUB>）诱导法制备胸主动脉瘤模型,于术后4周取外敷CaCl2段胸主动脉。HE染色及地衣红染色观察胸主动脉组织学改变;免疫组织化学和免疫印迹法检测动脉瘤壁VEGF和TSP-1的表达。结果 免     

脱氢表雄酮抑制高脂诱导的兔主动脉及人脐静脉内皮细胞细胞间黏附分子1的表达

目的:探讨脱氢表雄酮对高脂诱导的兔主动脉及人脐静脉内皮细胞细胞间黏附分子1(ICAM-1)表达的影响,以及全反式维甲酸(ATRA)在这一过程中的作用。方法:细胞实验:将培养的人脐静脉内皮细胞(HUVECs)分为正常对照组、氧化型低密度脂蛋白(ox-LDL)组、ox-LDL+DHEA组、ox-LDL+DHEA+ATRA组和DHEA组。各组细胞均加入相应药物作用24 h,采用RT-PCR和细胞酶联免疫吸附法检测各组细胞ICAM-1 m RNA及蛋白的表达情况。动物实验:将大耳白兔分为正常对照组、高脂组、高脂+DHEA组、高脂+DHEA+ATRA组和DHEA组。各组白兔均用相应饲料喂饲10周后处死动物,采用RT-PCR和免疫组织化学等方法检测各组白兔主动脉ICAM-1的m RNA及蛋白的表达情况。结果:细胞实验:ox-LDL组ICAM-1的表达明显高于正常对照组(P0.05);与ox-LDL组相比,ox-LDL+DHEA组ICAM-1的表达明显降低(P0.05);DHEA组与正常对照组ICAM-1的表达无显著差异(P0.05);ox-LDL+DHEA+ATRA组与ox-LDL+DHEA组ICAM-1的表达无显著差异(P0.05)。动物实验:高脂组主动脉ICAM-1的表达明显高于正常对照组(P0.05);与高脂组相比,高脂+DHEA组ICAM-1的表达明显降低(P0.05);DHEA组与正常对照组ICAM-1的表达无显著差异(P0.05);高脂+DHEA+ATRA组与高脂+DHEA组ICAM-1的表达无显著差异(P0.05)。结论:DHEA能够抑制高脂诱导的兔主动脉及人脐静脉内皮细胞ICAM-1的表达,这可能是其抗动脉粥样硬化的机制之一,而全反式维甲酸对DHEA的这一作用并无明显增强作用。     

同型半胱氨酸硫内酯-内质网应激途径促进HUVECs黏附

目的探讨同型半胱氨酸硫内酯(HTL)通过内质网应激途径促人脐静脉内皮细胞(HUVECs)黏附的可能机制。方法取HTL处理的大鼠胸主动脉,检测NF-κB p65的表达;用Western blot检测HUVECs中HTL,分别对其进行时效与量效处理后,所谓检测内质网应激蛋白Bip和Chop及黏附蛋白VCAM-1和ICAM-1的表达,以及内质网应激激动剂与抑制剂对HTL诱导的HUVECs黏附因子表达的影响;用"STRING"预测Bip(HSPA5)和Chop(DDIT3)与黏附因子VCAM-1和ICAM-1的相互作用。结果 HTL诱导大鼠胸主动脉血管的内皮细胞NF-κB p65表达,促HUVECs的内质网应激蛋白Bip和Chop及黏附因子VCAM-1和ICAM-1的表达(P0.05),内质网激动剂上调HTL对黏附因子的表达,内质网抑制剂抑制HTL对黏附因子的表达(P0.05);"STRING"软件预测内质网应激蛋白Bip和Chop与黏附因子VCAM-1和ICAM-1具有相互作用。结论 HTL可能通过内质网应激途径促进HUVECs黏附。     

硫化氢抑制apoE基因敲除小鼠动脉粥样硬化中ICAM-1的表达

目的　探讨硫化氢(H2S)对apoE基因敲除小鼠(apoE-/-小鼠)动脉粥样硬化中细胞间黏附分子-1 (ICAM-1)的调节作用。方法　6周龄雄性C57BL/6J和apoE-/-小鼠分为C57BL/6对照组、apoE-/-组、apoE-/-+硫氢化钠(NaHS)组和apoE-/-+炔丙基甘氨酸(PPG)组,每组各8只,普通饮食饲养10周。硫电极法测定血清中H2S的含量;ELISA法测定血清中ICAM-1的含量;荧光实时定量RT-PCR法测定主动脉组织中ICAM-1 mRNA的表达。油红O染色观察小鼠主动脉根部斑块面积的变化。结果 与C57BL/6J小鼠相比,apoE-/-小鼠血清中H2S的含量明显下降(P 0.01),血清中ICAM-1的含量和主动脉组织中ICAM-1 mRNA的表达明显升高(P 0.01),主动脉根部出现明显斑块;给予NaHS后,apoE-/-小鼠血清中H2S的含量明显升高(P 0.05),血清和主动脉组织中ICAM-1的表达明显降低(P 0.01和P 0.05),动脉粥样斑块明显缩小(P 0.05);给予PPG后,apoE-/-小鼠血清中H2S的含量明显降低(P 0.05),血清和主动脉组织中ICAM-1的表达明显增高(P 0.05和P 0.01),动脉粥样斑块明显增大(P 0.01)。结论　气体信号分子H2S可明显抑制动脉粥样斑块形成过程中ICAM-1的表达与分泌。     

瑞舒伐他汀对大鼠脑缺血再灌注ICAM-1和VCAM-1表达的抑制作用

目的观察大鼠脑缺血再灌注损伤后脑组织中细胞间黏附分子-1(ICAM-1)和血管间黏附分子-1(VCAM-1)的表达及瑞舒伐他汀干预对其影响。方法 SD大鼠随机分为3组:假手术组(sham组)、模型组(model组)和治疗组(test组)。治疗组在模型制作前用5 mg/(kg·d)瑞舒伐他汀连续灌胃10 d,1次/d。制作大鼠脑缺血再灌注损伤模型,缺血2 h再灌注24 h后,应用免疫组化法、RT-PCR法和Western blot法检测脑组织中ICAM-1和VCAM-1的表达。结果脑缺血再灌注损伤后,脑组织中ICAM-1和VCAM-1的表达明显增加,与假手术组相比有统计学意义(P0.05);瑞舒伐他汀干预后,能够显著降低脑组织中ICAM-1和VCAM-1的表达,与模型组相比有统计学意义(P0.05)。结论瑞舒伐他汀可抑制大鼠脑缺血再灌注损伤后脑组织中ICAM-1和VCAM-1的表达。     

姜黄素对大鼠胸主动脉瘤Bcl-2和Bax表达的影响

目的 探讨姜黄素对大鼠胸主动脉瘤形成过程中Bcl-2和Bax表达的影响。方法 将30只成年雄性Wistar大鼠随机分为3组,即对照组、动脉瘤组和姜黄素治疗组。采用氯化钙（CaCl2）诱导法制备胸主动脉瘤模型,术后4周取材。HE染色及地衣红染色观察胸主动脉组织学改变;免疫组织化学和Western blotting方法检测动脉瘤壁Bcl-2和Bax的表达。结果 姜黄素可明显抑制胸主动脉的扩张。与对照组比较,动脉瘤组Bax表达水平明显升高,Bcl-2表达水平降低,姜黄素能有效降低动脉瘤中Bax的表达,升高Bcl-2表达水平。 结论 姜黄素可以促进胸主动脉瘤Bc1-2蛋白的表达,抑制Bax蛋白的表达,降低Bax/Bcl-2的比值。     

JNK/c-Jun信号通路在大鼠胸主动脉瘤模型中的表达及意义

目的 探讨c -Jun氨基末端激酶(JNK)及c-Jun在实验性大鼠胸主动脉瘤中的表达及其意义. 方法 将20只成年雄性Wistar大鼠随机分为两组,即对照组和手术组.采用氯化钙(CaCl2)诱导法制备胸主动脉瘤模型,于术后4周取外敷CaCl2段胸主动脉.用免疫组织化学和Western blotting方法检测动脉瘤壁JNK和c-Jun的表达. 结果 免疫组织化学显示,磷酸化JNK(p-JNK)和磷酸化c-Jun( p-c-Jun)主要表达于动脉瘤中膜,而对照组表达很弱.Western blotting显示,动脉瘤组织中p-JNK和p-c-Jun表达均强于对照组. 结论 p-JNK和p-c-Jun在动脉瘤中表达强于对照组,JNK/c-Jun信号通路可能在动脉瘤形成过程中起重要作用.     

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...     

免疫球蛋白超家族黏附分子在淋巴管和不同血管内皮细胞的表达

目的比较免疫球蛋白超家族黏附分子在淋巴管、大血管和微血管内皮细胞的表达特点，探讨免疫球蛋白超家族黏附分子在淋巴管内皮细胞表达的意义。方法从狗的胸导管、颈总动脉、颈内静脉、肺微血管分离内皮细胞，利用免疫荧光标记法检测PECAM-1、ICAM-1、ICAM-3、VCAM-1和CD44在各种内皮细胞的表达，在荧光显微镜和激光共聚焦扫描显微镜下观察，并用图像分析仪分析表达强度。结果动脉、静脉和肺微血管内皮细胞表达PECAM—1、ICAM—1、ICAM-3、VCAM—1和CD44。其中，ICAM-1和ICAM-3的表达较弱。VCAM—1在动脉和肺微血管内皮细胞的表达比静脉强。淋巴管内皮细胞表达PECAM—1、ICAM—1、ICAM-3和CD44，未观察到VCAM—1的表达。ICAM-3和CD44的表达比血管内皮细胞强。结论与动脉、静脉和微血管内皮细胞比较，淋巴管内皮细胞不表达VCAM—1，而ICAM-3和CD44表达较强，这有助于解释淋巴细胞和肿瘤细胞与淋巴管内皮的黏附以及淋巴管新生的机制。     

Application of stereological methods for the quantification of VCAM-1 and ICAM-1 expression in early stages of rabbit atherogenesis

Early stages of atherogenesis are characterized by the overexpression of cell adhesion molecules with the subsequent accumulation of macrophages, smooth muscle cells and proliferation of extracellular matrix in arterial intima. The quantification of atherogenic changes is necessary for the objective evaluation of the atherogenic process. The purpose of this study was to introduce stereological methods that may be used for the quantification of immunohistochemical staining, namely intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Twenty-four New Zealand White rabbits were subdivided into the three groups. Eighteen rabbits received a 0.4% cholesterol diet for 1, 2 and 3 months, respectively. Stereological principles of the systematic uniform random sampling and the point-counting method were applied for the quantification. Stereological analysis showed that VCAM-1 and ICAM-1 were upregulated during the consumption of high cholesterol diet and that VCAM-1, but not ICAM-1, has a considerable role in the formation of early atherosclerotic lesions. Stereological methods proved to be useful for the quantification of immunohistochemistry and can be used for an objective characterization of atherogenic changes in atherosclerosis.     

七氟烷对心肌缺血再灌注内皮细胞细胞间黏附分子-1、血管细胞黏附分子-1和E-选择素表达的影响

目的： 探讨七氟烷对心肌缺血再灌注内皮细胞促炎作用的细胞间黏附分子-1（ ICAM-1）、血管细胞黏附 分子-1（ VCAM-1）和E- 选择素表达的影响。方法 ：在大鼠心肌缺血再灌注模型的基础上,将大鼠随机分为假 手术组（ 对照组）、缺血再灌注损伤组（ I/R 组）和七氟烷组;观察各组大鼠手术前、缺血15 min 和再灌注4 h 的 心率、平均动脉压和心率-收缩压乘积（ RPP ）;免疫组织化学法检测心肌组织中CD68+ 巨噬细胞数目、内皮细胞 ICAM-1、VCAM-1 和E- 选择素的表达;TUNEL 染色法检测凋亡细胞的比例。结果：缺血15 min 时,I/R 组和 七氟烷组平均动脉压和RPP 均显著下降;再灌注4 h 时,七氟烷组平均动脉压和RPP 均有所上升,相对于I/R 组, 差异具有统计学意义;与对照组比较,I/R 组内皮细胞ICAM-1、VCAM-1 和E- 选择素的表达均显著升高,七氟 烷则能够有效抑制I/R 引起的内皮细胞促炎分子的表达;对照组CD68+ 巨噬细胞为5.83 个/ 高倍镜视野（ HPF）, I/R 组数目为55.67 个/HPF,两组间差异具有统计学意义;七氟烷能够显著减少心组织内巨噬细胞的浸润,与I/R 组比较,降低了66.46%;TUNEL 染色结果显示对照组心肌细胞凋亡率2.20%,I/R 组为28.63%,两组间差异明显; 七氟烷能够显著降低心肌细胞的凋亡,相对于I/R 组,降低了51.76%。结论：七氟烷可降低缺血再灌注损伤后内 皮细胞表面促炎分子的表达,减少心肌组织巨噬细胞浸润和细胞凋亡。     

Progress in computer-generated three-dimensional reconstruction

The expression of PECAM, ICAM-1, VCAM-1, and E-selectin was studied in 64 samples of human coronary arteries taken from 15 explanted hearts obtained within 5 min of transplantation. Normal artery (n=12), predominantly fibrous plaques (n=23), and plaques containing extracellular lipid (n=26) and three segments showing recanalization channels were studied. All endothelial cells strongly and equally expressed PECAM; positive staining was used to check that artefactual denudation of the endothelial surface had not occurred. PECAM was also present in some lipid-filled macrophages. Normal arteries showed no VCAM-1 staining but focal segments of the endothelium were positive for ICAM-1 and E-selectin. ICAM-1 was strongly and constantly expressed by the endothelium over all types of plaques and in macrophages. E-selectin expression was confined to endothelial cells and occurred on the surface in 35 per cent of fibrous and 22 per cent of lipid-containing plaques. VCAM-1 staining of surface endothelium occurred in 39 per cent of fibrous and 20 per cent of lipid-containing plaques. A population of spindle-shaped cells of macrophage type (positive for EMB11 antigen) expressed VCAM-1 in lipid-containing plaques. Adventitial vessels adjacent to plaques showed endothelial expression of ICAM-1 and E-selectin. VCAM-1 staining of adventitial vessel endothelium was associated with local lymphoid aggregation. In conclusion, the expression of cell adhesion molecules is an important element in the inflammatory component of atherosclerosis and contributes to both monocyte and lymphocyte activation and recruitment from advential vessels and the arterial lumen.     

Patterns of myocardial cell adhesion molecule expression in human endomyocardial biopsies after cardiac transplantation. Induced ICAM-1 and VCAM-1 related to implantation and rejection.

Conflicting patterns of myocardial cell adhesion molecule expression associated with cardiac rejection have emerged from numerous studies of randomly selected cardiac biopsies. We designed a prospective, longitudinal study which reports both qualitative and quantitative levels of myocardial ICAM-1, VCAM-1, E-selectin, and P-selectin expression in sequential human cardiac allograft biopsies. Intense ICAM-1 and VCAM-1 staining was found in all biopsies during the first three weeks after transplant and coincided with elevated serum levels of troponin T, a sensitive marker of ischemic myocyte injury. Baseline ICAM-1 and VCAM-1 expression returned within three to four weeks, as did serum troponin T levels in all patients who did not develop rejection. All 29 rejection episodes encountered were associated with intense ICAM-1 staining, while 24 of the 29 (83%) had intense VCAM-1 staining. Increased ELAM-1 and CD62 staining was only rarely observed. Persistence of increased ICAM-1 and VCAM-1 staining after treated rejection episodes predicted a recurrent rejection episode within two months (75% positive and 100% negative predictive value). Objective quantitative measurements by radioimmunoassay (RIA) confirmed these patterns of induced ICAM-1 and VCAM-1 expression. Thus, longitudinal monitoring of serial biopsies for myocardial ICAM-1 and VCAM-1 expression could be useful in the early detection of rejection episodes and monitoring the efficacy of immunosuppressive therapy.     

氟伐他汀单用及与安体舒通联用对兔相关炎症因子及基质金属蛋白酶-9的影响

目的探讨他汀类药物单用及联用醛固酮拮抗剂安体舒通对兔颈动脉组织ICAM-1、VCAM-1及MMP-9表达的影响。方法高脂饲养兔建立动物模型。96只新西兰兔分为对照组、高脂饮食组、氟伐他汀处理组（氟伐他汀组）以及氟伐他汀与安体舒通联合处理组（联合处理组）,每组24只。用免疫组织化学法检测ICAM-1、VCAM-1、MMP-9表达量。结果氟伐他汀组和联合处理组ICAM-1、VCAM-1及MMP-9的表达随时间的增加而逐渐降低（P〈0.05）,且在治疗8周和12周时降低较为显著（P〈0.05）。结论随着高脂饲养时间的延长,动脉组织中ICAM-1、VCAM-1及MMP-9表达量增加;他汀类药物可降低ICAM-1、VCAM-1及MMP-9表达量,延缓动脉粥样硬化形成及易损组织产生,联合醛固酮拮抗剂时此作用增强。