依达拉奉联合灯盏花素对脑缺血大鼠大脑皮质MCP-1的影响

目的　观察大鼠脑缺血（MCAO）后大脑皮质MCP-1的表达变化以及用依达拉奉联合灯盏花素干预后对MCP-1表达的影响。 方法　复制大鼠大脑中动脉闭塞（MCAO）模型,应用RT-PCR、Western blot和免疫荧光技术检测大鼠MCAO及药物干预后MCP-1的表达变化。 结果　RT-PCR显示大鼠MCAO后大脑皮质MCP-1 mRNA的表达比对照组显著上升（P<0.05）,12 h达高峰,与1 d、3 d及1周组比有显著差异（P<0.05）;给予两种药物联合处理后,mRNA表达显著降低,与对照组及单独用药组相比均有显著差异（P<0.05）。 Western blot显示MCAO 1 d、3 d、1周大脑皮质MCP-1蛋白的表达显著增强,与对照组比有显著差异（P<0.05）;两种药物联合处理后,MCAO大鼠大脑皮质MCP-1蛋白表达明显减少,与对照组及单独用药相比均有显著差异（P<0.05）。免疫荧光染色显示MCAO大鼠缺血半暗带有大量激活小胶质细胞,一部分与MCP-1免疫阳性细胞有共表达,其中MCAO后1周组最明显。 结论　大鼠局灶性脑缺血（MCAO）后,依达拉奉联合灯盏花素治疗能有效减少大脑皮质MCP-1的表达,效果优于两种药物单独使用。     

细胞间粘附分子-1和血管细胞间粘附分子-1的结构与功能

细胞粘附分子（ｃｅｌｌ　ａｄｈｅｓｉｏｎ　ｍｏｌｅｃｕｌｅ，　ＣＡＭ）是一类调节细胞与细胞、细胞与细胞外基质（ｅｘｔｒａｃｅｌｌｕｌａｒ　ｍａｔｒｉｘ，　ＥＣＭ）间相互结合、起粘附作用的膜表面糖蛋白。细胞间粘附分子－１（ｉｎｔｅｒｃｅｌｌｕｌａｒ　ａｄｈｅｓｉｏｎ　ｍｏｌｅｃｕｌａｒ－１，　ＩＣＡＭ－１）和血管细胞间粘附分子－１（ｖａｓｃｕｌａｒ　ｃｅｌｌ　ａｄｈｅｓｉｏｎ　ｍｏｌｅｃｕｌａｒ－１，　ＶＣＡＭ－１）均属于ＣＡＭ中免疫球蛋白超家族（ｉｍｍｕｎｏｇｌｏｂｕｌｉｎ　ｓｕｐｅｒｆａｍｉｌ…     

脑室和腹腔注射灯盏花素对大鼠脑缺血再灌注损伤的保护

目的探讨脑室直接灌注灯盏花素注射液，对大鼠脑缺血再灌注损伤的保护作用。方法采用线栓法制备大鼠大脑中动脉缺血再灌注模型，在再灌注后的不同时间点（3h、6h、24h）；通过脑室直接灌注、腹腔注射和脑室灌注＋腹腔注射的方式使用灯盏花素，观察用药后大鼠神经功能和组织病理学改变，计算脑梗死体积比、脑水肿体积和脑含水量。结果与对照组相比，灯盏花素组的脑梗死体积比、脑水肿体积和脑含水量均明显减轻，随着缺血时间的延长，这种保护作用逐渐降低，脑室灌注＋腹腔注射联合使用的保护效果明显优于单纯脑室灌注或腹腔注射给药。结论脑缺血再灌注后使用灯盏花素具有明显的神经功能保护作用，脑室灌注和腹腔注射给药的保护作用相似，但在损伤后的早期（〈6h）、超早期（〈3h）采用脑室灌注＋腹腔注射联合给药的方式效果最佳。     

灯盏花素对大鼠心室肌细胞钠通道的影响

目的： 研究灯盏花素对大鼠心室肌细胞膜钠通道的影响,在离子通道水平探讨灯盏花素的抗心律失常作用机制。方法： 用急性酶解法获得单个大鼠心室肌细胞,标准的全细胞膜片钳技术记录钠通道电流(INa)。结果： (1) 灯盏花素呈浓度依赖性抑制INa,在-30 mV时,含1、3、30、100 mg·L-1灯盏花素的细胞外液分别灌流细胞3 min,分别阻断INa峰电流(7.98±0.60)%、(37.73±2.31)%、(65.58±2.90)% 和(88.09±5.60)%。INa激活电位为-70 mV,最大峰电位为-30 mV,翻转电位为5 mV,激活和失活过程呈电压和时间依赖性。30 mg·L-1灯盏花素使电流电压曲线明显上移,峰值电流从（13.49±1.25）pA/pF 减少至（4.78±0.85）pA/pF,n=8,P<0.05,冲洗后可以不完全恢复。（2）灯盏花素能使钠电流失活曲线明显左移。（3）灯盏花素使钠电流激活曲线明显右移。（4）灯盏花素使钠电流复活明显减慢。结论： 灯盏花素能够抑制心肌细胞钠通道电流,并呈浓度依赖性。     

细胞间粘附分子-1与病毒性肝炎

目前在粘附分子家族的研究中，以细胞间粘附分子-1的研究最为深入，本文对其在，病毒性肝炎中的表达与调节，血清中可溶性细胞间粘附分子-1的水平与来源，以及它们在肝炎发病中的意义等有关情况作一简介。     

细胞间粘附分子—1在不同白血病细胞表面的表达

细胞间粘附分子 1(ＩＣＡＭ 1)属于免疫球蛋白超基因家族 ,是 β2亚家族淋巴细胞相关功能抗原(ＬＦＡ 1)的配体。正常生理功能为淋巴细胞活性提供重要的共刺激信号及调节淋巴细胞迁移。以前我们的研究显示ＬＦＡ 1在各种淋巴增殖性疾病存在异常表达及与疾病的发生、发展有关[1] ,本文进一步观察其配体细胞间粘附分子 1(ＩＣＡＭ 1)在各种白血病细胞的表达及其与临床特征、疗效的关系。1　材料与方法1 1　研究对象　 34例初治或复发急性淋巴细胞白血病 (ＡＬＬ)患者 ,男 18例 ,女 16例 ,中位年龄 32 (17～ 5 8)岁 ,按本免疫室建立的方法进…     

灯盏花素对大鼠出血性脑损伤的保护作用

目的:探讨灯盏花素注射液对大鼠出血性脑损伤的保护作用。方法:用胶原酶和肝素混合液注入大鼠尾壳核建立脑出血(ICH)模型,然后将大鼠随机分为对照组、模型组和治疗组。治疗组动物于注射灯盏花素注射液后第3、5、7 d后处死。应用Berdson评分标准对各组大鼠进行神经功能评分,应用免疫组织化学方法检测出血灶周围TNF-α和IL-8的表达,应用流式细胞术检测神经细胞凋亡率。结果:与模型组比较,治疗组大鼠神经功能评分明显增加(P<0.05);灯盏花素治疗组脑细胞的凋亡率明显减低(P<0.05);治疗组出血灶周围炎症因子TNF-α,IL-8明显减少(P<0.05);结论:灯盏花素注射液能保护神经元,促进神经功能恢复。     

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。     

血管细胞粘附分子与细胞间粘附分子在大鼠骨髓间充质干细胞中的表达及意义

目的:探讨血管细胞粘附分子(VCAM-1)与细胞间粘附分子(ICAM-1)在体外培养大鼠骨髓间充质干细胞(rMSCs)中的表达.方法:采用直接贴壁法获得rMSCs;用免疫细胞化学方法从蛋白水平对VCAM-1和ICAM-1进行定位分析,采用免疫荧光直标法在流式细胞仪上检测VCAM-1、ICAM-1抗原的表达率;RT-PCR法从mRNA水平对VCAM-1和ICAM-1进行半定量分析.结果:免疫细胞化学显色显示, VCAM-1表达弱阳性,而ICAM-1表达强阳性;流式细胞仪检测显示,VCAM-1的表达率14.9%,而ICAM-1的表达率为100%;RT-PCR显示,VCAM-1的mRNA呈微弱表达,ICAM-1的mRNA呈强表达.结论:体外培养下,rMSCs VCAM-1低表达,而ICAM-1高表达,为进一步研究骨髓MSC在细胞替代治疗等临床应用提供参考.     

依达拉奉联合灯盏花素对局灶性脑缺血大鼠皮层神经元凋亡的影响

目的:探讨依达拉奉联合灯盏花素(简称灯盏花素)治疗对大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)模型大鼠局灶性脑缺血后大脑皮层神经细胞凋亡的影响。方法:将25只SD大鼠随机分为5组:假手术组、MCAO组、MCAO+依达拉奉组、MCAO+灯盏花素组、MCAO+依达拉奉+灯盏花素(n=5),应用微创开颅法制作大鼠MCAO模型,药物组于术前2 h,术后12、24、36、48、60 h经腹腔注射依达拉奉5 mg/kg,灯盏花素100 mg/kg,依达拉奉+灯盏花素(5 mg/kg+100 mg/kg)。假手术组和MCAO组均给予生理盐水。各组分别于术后1 d、3 d和7 d断头取脑,制备常规石蜡组织切片。应用神经功能缺损评分法评估大脑缺血后的神经功能。利用尼氏染色观察不同时间点脑缺血大鼠大脑皮层神经元的形态和数量变化。采用TUNEL方法显示脑缺血后细胞凋亡。应用免疫组织化学法检测凋亡相关蛋白Bcl-2和Bax在脑缺血大脑皮层中的表达变化。结果:(1)大鼠脑缺血后神经功能缺损评分结果显示:假手术组大鼠神经功能正常;MCAO组大鼠神经功能评分在不同点显著增高于假手术组(P0.05);MCAO+依达拉奉+灯盏花素组大鼠神经功能评分在10 d、14 d较依达拉奉组、灯盏花素组明显降低,与单药组相比差异有统计学意义(P0.05),但各时间点均高于假手术组(P0.05)。(2)假手术组大鼠脑缺血大脑皮层尼氏染色和TUNEI检测显示依达拉奉+灯盏花素组各时间点大脑皮层核固缩神经元及凋亡细胞与两种药物单独使用相比数量明显减少(P0.01)。(3)免疫组化结果显示:依达拉奉+灯盏花素组缺血侧大脑皮层Bcl-2阳性细胞表达显著增强,Bax阳性细胞表达明显减少、减弱,与单独用药相比差异有统计学意义(P0.01)。结论:依达拉奉联合灯盏花素治疗大鼠脑缺血可能通过增强/抑制神经元凋亡相关蛋白Bcl-2/Bax的表达,提高Bcl-2/Bax的比值,抑制神经细胞凋亡和增强神经元的抗凋亡作用,对缺血脑组织发挥神经保护作用。     

Interleukin-10 inhibits B7 and intercellular adhesion molecule-1 expression on human monocytes

There is evidence that interleukin ?10(IL-10) interferes with the costimulatory properties of antigen-presenting cells and, thereby, inhibits their ability to induce T cell activation. To determine whether this effect might involve modulation of the expression of accessory molecules, we analyzed by flow cytometry the influence of human IL-10 on the basal expression of intercellular adhesion molecule 1 (ICAM-1) as well as on the interferon γ(IFN-γ)-induced up-regulation of ICAM-1 and B7 at the surface of human monocytes. IL-10 inhibited both the basal expression and the IFN-γ-induced ICAM-1 up-regulation. IL-10 also reduced B7 up-regulation on IFN-γ-stimulated monocytes. The inhibitory effect of IL-10 both on ICAM-1 and B7 expression was shown to be dose dependent. We conclude that the ability of IL-10 to decrease both ICAM-1 and B7 expression on monocytes might contribute to its immunosuppressive properties.     

Immunohistochemical analysis of intercellular adhesion molecule-1 expression in human gastric adenoma and adenocarcinoma

In this study, we examined the distribution of intercellular adhesion molecule-1 (ICAM-1) in gastric adenomas and carcinomas immunohistochemically at the light and electron microscopic levels. ICAM-1 was expressed on tumour cells in 12 of 28 gastric carcinomas and in 3 of 11 adenomas but not on most normal gastric epithelial cells. ICAM-1 was localized on luminal sites of neoplastic glands in adenomas and in intestinal-type carcinomas, and rarely on the surface of tumour cells of diffuse carcinomas. Expression of ICAM-1 on the tumour cells was more frequent in intestinal-type than diffuse carcinomas (P<0.005). At the ultrastructural level, ICAM-1 was present prominently on the apical membrane and weakly on the lateral surface of the tumour cells of the intestinal-type carcinoma and also localized on the perinuclear membrane and the membrane of the endoplasmic reticulum of cancer cells. There was no significant association between. ICAM-1 expression and HLA antigen expression or the number of infiltrating lymphocyte subsets. These results may implicate the synthesis of ICAM-1 by gastric cancer cells, but the expression is infrequent and may not be sufficient for host immune surveillance of the tumour cell.     

ICAM-1与支气管哮喘的研究进展

细胞间粘附分子-1(intercellularadhesionmolecule-1,ICAM-1)是免疫球蛋白(immunoglobulin,Ig)超家族成员之一,对白细胞牢固黏附和白细胞从血管中迁移到炎症组织部位起着关键作用.白细胞表面粘附分子与血管内皮细胞表面的粘附分子(如:ICAM-1)相互作用后可介导白细胞从血液循环中迁移到肺组织的炎症部位,这在支气管哮喘发病机制中起着重作用.本综述将简阐述ICAM-1及其表达调控在支气管哮喘中的研究进展.     

急性脑梗死患者血清sICAM-1含量变化的研究

目的 :探讨人类脑缺血后血流中可溶性细胞间粘附分子 1(sICAM 1)含量与疾病转归、脑血管病危险因素及病变体积的关系。方法 :采用酶联免疫吸附法 ,测定 35例脑梗死患者血清sICAM 1的含量 ,与 2 0例正常人对照比较。结果 :脑梗死4 8h内和 14d血清sICAM 1含量明显高于正常对照组 (P <0 0 5 ,P <0 0 0 5 )。脑梗死 4 8h内 ,合并高血压、糖尿病患者血清sICAM 1明显高于非高血压、糖尿病患者 (P <0 0 5 ;P<0 0 0 1) ,且血清sICAM 1的含量与血糖水平有明显相关性 (r=0 8857,P <0 0 5 )。动态观察显示 ,脑梗死 4 8h内与 14d血清sICAM 1含量比较无明显变化 ,但血清sICAM 1含量与单发梗死体积有明显相关性 (r=0 4 38,P <0 0 5 ;r=0 5 37,P <0 0 5 )。结论 :ICAM 1与脑梗死的发生发展密切相关 ,其含量受脑血管病危险因素、梗死体积等多种因素影响     

Soluble intercellular cell adhesion molecule-1 in lung cancer: A meta-analysis

BackgroundMany recent studies have investigated the prognostic, diagnostic, and progressive features of soluble intercellular cell adhesion molecule-1 (sICAM-1) in lung cancer patients, but the results remained inconsistent. This study aimed to explore the value of serum sICAM-1 in patients with lung cancer.MethodsA comprehensive systematic literature search in the Wanfang databases, china national knowledge infrastructure, Pubmed, and Embase was carried out update to June 15, 2019. The standard mean difference (SMD), hazard ratio (HR), and 95% confidence interval (95% CI) were applied to investigate the effect sizes.Results23 observational studies were included. According to our results, the serum sICAM-1 concentrations in patients with lung cancer were significantly higher than that in controls (healthy controls: SMD: 4.08, 95% CI: 3.14–5.02, P < 0.001; benign lung diseases controls : SMD: 1.48, 95% CI: 0.23–2.73,P = 0.02). Fortunately, a subgroup analysis was performed by language, treatment status, and lung cancer types, and the statistical results were similar. Serum sICAM-1 levels were markedly higher in stage III/IV than stage I/II (SMD: 1.96, 95% CI: 1.08−2.84, P < 0.001), Additionally, lung cancer patients with lymph node metastasis had a higher concentrations of serum sICAM-1(SMD: 1.83, 95% CI: 0.95−2.72, P < 0.001), as well as with distant metastasis (SMD: 0.86, 95% CI: 0.47−1.25, P < 0.001). Additionally, patients with higher sICAM-1 levels were related to a significantly poorer prognosis (progression free survival: HR: 1.16, 95% CI: 1.07–1.26, P < 0.001; overall survival: HR: 1.45, 95% CI: 1.17–1.79, P = 0.001).ConclusionsOur study suggested that serum sICAM-1 levels may act as a potential marker for diagnosing lung cancer and predicting its staging, and were negatively correlated with prognosis of lung cancer.     

促红细胞生成素对大鼠脑缺血再灌注损伤的保护作用及细胞黏附分子-1表达的影响

目的:观察促红细胞生成素(EPO)预处理对大鼠局灶性脑缺血再灌注后脑组织的病理变化和细胞黏附分子-1(ICAM-1)表达的影响,探讨其保护作用.方法: 96只SD大鼠随机分为对照组、假手术组、模型组、EPO组,分设4个时间点的亚组,每亚组6只.采用Longa线栓法制备大鼠大脑中动脉阻塞2 h模型,再灌注6、24、48、96 h后行神经功能评分,H-E染色观察病理学变化,免疫组织化学方法测定各组ICAM-1阳性反应细胞.结果:24 h开始EPO组神经功能评分改善,神经细胞存活数量增多,损伤程度减轻,而且减少了各时间点脑组织中ICAM-1阳性细胞表达.结论: EPO处理可抑制缺血侧皮层的神经细胞变性坏死,其保护机制可能与脑缺血再灌注后炎症因子ICAM-1表达减少有关.     

巨噬细胞浸润及细胞间粘附分子-1表达在油酸致大鼠急性肺损伤发病中的作用

目的:探讨巨噬细胞浸润及细胞间粘附分子-1(ICAM-1)表达在油酸诱导的大鼠急性肺损伤(ALI)中的作用。方法:雄性Wistar大鼠静脉注射油酸复制ALI为油酸组,静脉注射生理盐水为对照组。静注后4h,测定血气(左心PaO₂)、肺泡通透指数等肺损伤指标。支气管肺泡灌洗液(BALF)中巨噬细胞比和可溶性细胞间粘附分子-1(sICAM-1)水平。用原位杂交检测ICAM-1mRNA表达水平和免疫组化双重套染方法检测巨噬细胞浸润程度与ICAM-1表达的关系。结果:油酸组PaO₂低于对照组、肺泡通透性指数高于对照组(P＜0.01),BALF中巨噬细胞比例,sICAM-1水平显著高于对照组(P＜0.01)。油酸组肺组织ICAM-1表达明显高于对照组,且肺组织中巨噬细胞浸润数、ICAM-1表达水平和肺损伤指标呈显著正相关。结论:巨噬细胞浸润在油酸致急性肺损伤中起重要作用,ICAM-1参与介导了巨噬细胞对组织的粘附、浸润和ALI的发生发展。     

细胞间黏附分子-1与血管生成的研究进展

实体肿瘤的生长、浸润和转移均依赖于血管生成这一进程,而血管生成是在一系列生长因子调控下实现的。有资料显示,细胞间黏附分子-1与血管生成有关,它通过与内皮细胞表面上的特异性受体结合而发挥其生物学活性,在某些疾病过程中的血管生成及发生发展过程中起着重要作用。现就细胞间黏附分子-1的生物学特性及与血管生成的关系研究进展概述如下。     

Inhibition of intercellular adhesion molecule-1 (ICAM-1), soluble ICAM-1 and interleukin-4 by nitric oxide expression in migraine patients

 The mechanisms of the postulated ”sterile” inflammation in migraine were studied utilizing flow cytometry (intercellular adhesion molecule 1, ICAM-1; interleukin-1 receptor, IL-1R) and enzyme-linked immunosorbent assay (soluble intercellular adhesion molecule 1, sICAM-1; interleukin-4, IL-4). Twenty patients suffering from migraine without aura, 20 healthy subjects, and 10 patients suffering from episodic tension headache were selected. All of the migraine patients were studied during a migraine crisis experimentally induced by the administration of isosorbide dinitrate (a nitric oxide donor), and 10 out the 20 were also studied during a spontaneous migraine attack. A sharp decrease in the expression of ICAM-1 (F=5.09, p<0.001 and F=2.46, p<0.05, respectively), sICAM-1 1 (F=6.21, p<0.0001 and F=3.99, p<0.007, respectively) and serum IL-4 (F=6.23, p<0.001 and F=3.64, p<0.01, respectively) were observed in experimentally induced and spontaneous migraine attacks. There was no change with respect to IL-IR 1 receptor expression values. The two control groups, tested with the same experimental procedure, showed no changes in ICAM-1 and IL-1R or in in sICAM-1 and IL-4. Our data suggest that migraine patients are more sensitive to exogenous NO than controls. In addition, our results indicate that experimental migraine crisis, induced by an NO donor, is mediated by the inhibition of IL-4 and subsequently of ICAM-1. It is likely that the described ICAM-1 downregulation inhibits during a migraine attack the critical step of transendothelial migration into the cerebral tissues of activated leukocytes, as proposed in the ”sterile inflammation” hypothesis. Received: 17 April 1996 / Accepted: 30 December 1996