Increased binding of synovial T lymphocytes from rheumatoid arthritis to endothelial-leukocyte adhesion molecule-1 (ELAM-1) and vascular cell adhesion molecule-1 (VCAM-1).

The infiltration of the synovial membrane (SM) by mononuclear cells, mostly T cells, is a typical histopathological feature associated with rheumatoid arthritis (RA). The entry of T lymphocytes into the SM is believed to be mediated by a number of molecules in the endothelium that are induced in response to a series of inflammatory mediators. In this study, we have investigated the adhesion of synovial T cells from RA patients to two endothelial ligands: endothelial-leukocyte adhesion molecule-1 (ELAM-1), the only selectin known to function as a vascular addressin for T cells, and vascular cell adhesion molecule-1 (VCAM-1), the cellular ligand of VLA-4. Our results clearly demonstrate that synovial T cells isolated from both SM and synovial fluid (SF), bearing an activated and memory phenotype, displayed an enhanced capacity to interact with these two endothelial molecules as compared with T cells from peripheral blood (PB) either of the same RA patients or healthy donors. A further enhancement of VLA-4-mediated T cell binding to VCAM-1 and fibronectin could be observed when already in vivo-activated synovial T cells were stimulated in vitro with phorbol esters, suggesting the existence of several cellular affinity levels for both very late activation-4 (VLA-4) ligands. Moreover, both PB and synovial T cells from RA patients exhibited strong proliferative responses when they were cultured with either fibronectin or VCAM-1 in combination with submitogenic doses of anti-CD3 mAb. This increased endothelial binding ability of synovial T lymphocytes together with their proliferation in response to the interaction with VCAM-1 and fibronectin may represent important mechanisms in the regulation of T cell penetration and persistence in the chronically inflamed SM of RA.     

Expression of endothelial-leukocyte adhesion molecule-1 in elicited late phase allergic reactions.

To better understand the events involved in the local migration of inflammatory cells into sites of allergic reactions, we studied expression of the cytokine inducible endothelial cell (EC) neutrophil adhesion molecule, endothelial-leukocyte adhesion molecule (ELAM-1), in sequential skin biopsies from patients with respiratory allergy during the late phase reaction (LPR) between 20 min and until 24 h after intradermal allergen (ragweed or dust mites) injection. In 7 of 7 atopic patients but in only 1 of 4 apparently normal controls, allergen induced appearance of ELAM-1 on EC. ELAM-1 expression occurred concurrently with the development of inflammatory cell infiltrates by 3-4 h after intradermal injection. Saline injected sites in all subjects were negative. Skin organ cultures demonstrated that allergen could produce the same EC changes in vitro whether allergen was injected in vivo 20 min before culture or added during skin culture. These EC changes in organ culture were inhibited by the presence of combined anti-sera to both TNF-alpha and IL-1, but not by antisera to either cytokine alone. We conclude that EC activation occurs in elicited LPR and suggest that cytokine-induced EC activation may play a role in the migration of inflammatory cells into allergic skin reactions. Furthermore, resident cells in the skin rather than infiltrating leukocytes appear to be the source of the cytokines that mediate endothelial activation.     

Role of focal adhesion kinase in lung remodeling of endotoxemic rats

Despite significant advances in the care of critically ill patients, acute lung injury continues to be a complex problem with high mortality. The present study was designed to characterize early lipopolysaccharide (LPS)-induced pulmonary injury and small interfering RNA targeting focal adhesion kinase (FAK) as a possible therapeutic tool in the septic lung remodeling process. Male Wistar rats were assigned into endotoxemic group and control group. Total collagen deposition was performed 8, 16, and 24 h after LPS injection. Focal adhesion kinase expression, interstitial and vascular collagen deposition, and pulmonary mechanics were analyzed at 24 h. Intravenous injection of small interfering RNA targeting FAK was used to silence expression of the kinase in pulmonary tissue. Focal adhesion kinase, total collagen deposition, and pulmonary mechanics showed increased in LPS group. Types I, III, and V collagen showed increase in pulmonary parenchyma, but only type V increased in vessels 24 h after LPS injection. Focal adhesion kinase silencing prevented lung remodeling in pulmonary parenchyma at 24 h. In conclusion, LPS induced a precocious and important lung remodeling. There was fibrotic response in the lung characterized by increased amount in total and specific-type collagen. These data may explain the frequent clinical presentation during sepsis of reduced lung compliance, oxygen diffusion, and pulmonary hypertension. The fact that FAK silencing was protective against lung collagen deposition underscores the therapeutic potential of FAK targeting by small interfering RNA.     

神经激肽-1受体在急性坏死性胰腺炎肺损害中的作用

目的 :研究神经激肽 1受体 (NK 1R)在急性坏死性胰腺炎 (ANP)大鼠肺组织中的表达 ,探讨该受体在 ANP肺损害中的作用。方法 :健康成年 Sprague Dawley大鼠按抽签法随机分为 ANP组 (90只 )和正常对照组 (30只 )。正常对照组开腹后只翻动胰腺 ,ANP组大鼠经胰胆管恒速逆行注射质量分数为 5 %的牛磺胆酸钠 (0 .1ml/ kg)制成 ANP大鼠模型。检测肺脏髓过氧化物酶 (MPO)的活性和肺脏毛细血管通透性 (L CP)。应用逆转录聚合酶链反应 (RT PCR)检测肺组织中 NK 1R m RNA水平 ,应用 Western Blot技术检测NK 1R的蛋白水平 ,以免疫组织化学方法进行 NK 1R的组织学定位。结果 :ANP组 6 h后肺组织 MPO和L CP水平即明显高于正常对照组。与正常对照组相比 ,ANP肺组织中 NK 1R m RNA和蛋白都过度表达 ;NK 1R m RNA表达分别与 MPO(r=0 .83,P<0 .0 1)和 L CP(r=0 .79,P<0 .0 1)水平相关。免疫组织化学检测显示 ,NK 1R的表达主要位于肺泡隔血管内皮细胞表面及部分肺泡 型、 型上皮细胞表面等处。结论 :ANP肺组织中 NK 1R的表达水平明显上调 ,导致中性粒细胞等炎性细胞聚集 ,加剧 ANP时的肺损害。     

Chemotactic factors regulate lectin adhesion molecule 1 (LECAM-1)-dependent neutrophil adhesion to cytokine-stimulated endothelial cells in vitro.

Monoclonal antibodies recognizing CD18, CD11a, CD11b, and neutrophil lectin adhesion molecule 1 (LECAM-1), i.e., the human homologue of the murine MEL-14 antigen, were used to assess the relative contribution of these glycoproteins to neutrophil-endothelial adhesion. Under static conditions, the adhesion of neutrophils to IL-1-stimulated human umbilical vein endothelial cell (HUVEC) monolayers was inhibited by antibodies to CD18, CD11a, and the neutrophil LECAM-1, and the effect of combining anti-LECAM-1 and anti-CD11a was almost additive. Under flow at a wall shear stress 1.85 dyn/cm2, a condition where CD18-dependent adhesion is minimal, anti-LECAM-1 inhibited adhesion by greater than 50%. Chemotactic stimulation of neutrophils induced a rapid loss of LECAM-1 from the neutrophil surface, and the level of neutrophil surface LECAM-1 was closely correlated with adhesion under flow. Neutrophils contacting the activated endothelial cells for 30 min lost much of their surface LECAM-1, a phenomenon induced by a soluble factor or factors released into the medium by the stimulated monolayers, and a high percentage migrated through the HUVEC monolayer. This migration was almost completely inhibited by anti-CD18, but was unaffected by antibodies to neutrophil LECAM-1. These results support the concept that LECAM-1 is a neutrophil adhesion molecule that participates in the adherence of unstimulated neutrophils to cytokine-stimulated endothelial cells under conditions of flow, and is then lost from the neutrophil surface coincident with the engagement of CD18-dependent mechanisms leading to transendothelial migration.     

Dextran sulfate as a leukocyte-endothelium adhesion molecule inhibitor of lung injury in pediatric open-heart surgery

BACKGROUND: In spite of the progress in operative techniques and pre- and postoperative management for congenital heart disease, lung injury induced by the extracorporeal circulation is still a serious insult in pediatric open-heart operations. To prevent this injury, we used a leukocyte-endothelial cell adhesion molecule blocking agent, dextran sulfate, in a clinical setting. METHODS: Sixty mg/kg of dextran sulfate (DS) was intravenously infused to the patients just before cardiopulmonary bypass was started and 600 mg was added to the bypass circuit prime. Thirty patients (DS group, 14 patients with atrial septal defect, and 16 patients with ventricular septal defect) were compared with age and body-weight matched control patients (control group, 14 patients with atrial septal defect, 11 patients with ventricular septal defect). Postoperative respiratory index, white blood cell counts, complement C3 and plasma granulocyte elastase levels during and after the operation were measured. RESULTS: Respiratory index just after the termination of cardiopulmonary bypass was better preserved in the DS group than in the control group (0.50 +/- 0.08 versus 0.81 +/- 0.12, p < 0.01). The sum total amount of measured granulocyte elastase across whole study period was significantly lower in the DS group (p < 0.05). CONCLUSIONS: The data suggeste the possible effects of dextran sulfate in ameliorating post-perfusion lung damage by interfering with leukocyte-endothelial cell adhesion in pediatric open-heart operations. Future application to patients with more complex anomalies is anticipated.     

缺血性脑损伤神经再塑过程中神经细胞黏附分子的表达

目的：研究大鼠缺血性脑损伤后神经细胞黏附分子的表达对神经可塑性的影响。方法：Wistar大鼠26只，分为空白对照组（n=3）、假手术组（n=3）和损伤组（n=20）。对损伤组大鼠，使用线栓模型造成右侧大脑中动脉阻断（MCAO）。再灌1d(n=5)、2d(n=5)、3d(n=5)和7d(n=5)，用免疫组织化学的方法，测定脑片神经细胞黏附分子的表达。结果：损伤组4个时间点颞叶皮质都有神经细胞黏附分子表达的增加，以术后2d、3d明显，7d仍有较大量的表达。结论：在短暂缺血性脑损伤后，神经细胞黏附分子表达的增加可能与神经可塑性有关。     

中性粒细胞凋亡在大鼠急性肺损伤发病机制中的意义

目的从细胞凋亡的角度探讨急性肺损伤(ALI)的发病机制。方法雄性SD大鼠36只,随机分为模型组(ALI组)30只和正常对照组6只,观察肺组织病理切片,进行肺损伤评分(LIS)、肺水含量测定、肺通透性测定(LPI)、肺泡灌洗液(BALF)中肿瘤坏死因子-α(TNF-α)测定、BALF中性粒细胞(PMN)凋亡测定。结果模型组可见肺泡腔狭窄、炎性细胞渗出等ALI表现,且随时程延长病变加重。模型组各时相肺损伤评分较对照组有显著性差异(P均<0·05),随时程延长肺损伤评分逐渐增加。模型组各时相点肺湿干重比较对照组明显升高(P均<0·05),但各时相点之间无差异。模型组LPI2、4h与对照组无差异,6、8、16h显著升高(P均<0·01)。模型组2hBALF中TNF-α达高峰(P<0·01),4、6h与对照组有显著差异(P均<0·05),8、16h与对照组组无差异。BALF中PMN凋亡结果,模型组各时相点均低于对照组(P均<0·01)。结论PMN在肺泡内的凋亡在ALI的发生发展中起重要作用。ALI时BALF中PMN凋亡率呈下降的趋势,总体低于正常值。     

P选择素单克隆抗体对大鼠肝缺血—再灌注损伤的治疗作用研究

目的：探讨Ｐ选择素单克隆抗体（单抗）对大鼠肝缺血再灌注损伤的保护作用。方法：在肝缺血再灌注大鼠模型上观察了细胞间粘附分子１和Ｐ选择素的变化，并用Ｐ选择素单抗对其进行阻断治疗。结果：缺血再灌注大鼠肝细胞发生水肿及空泡变性，血清天冬氨酸转氨酶和丙氨酸转氨酶水平升高；但再灌注前５分钟经静脉注射Ｐ选择素单抗，则肝组织与正常组相近，肝细胞未见空泡变性，血清酶水平明显减低；酶联免疫吸附试验发现，再灌注后血清ＩＣＡＭ１和血浆Ｐ选择素水平显著升高，经Ｐ选择素单抗处理的大鼠血ＩＣＡＭ１和Ｐ选择素明显下降。结论：ＩＣＡＭ１和Ｐ选择素与缺血再灌注损伤密切相关，Ｐ选择素单抗对肝缺血再灌注损伤具有保护作用。     

Blocking of lung endothelial cell adhesion molecule-1 (Lu-ECAM-1) inhibits murine melanoma lung metastasis.

The 90-kD lung endothelial cell adhesion molecule-1 (Lu-ECAM-1) selectively promotes Ca(2+)-dependent adhesion of lung-metastatic B16 melanoma cells. Corresponding with their metastatic performance, high lung-metastatic B16-F10 melanoma cells bind in significantly higher numbers to Lu-ECAM-1 than their intermediate and low lung-metastatic counterparts B16-L8-F10 and B16-F0, respectively. Maximum attachment is observed at a density of approximately 2.4 x 10(2) Lu-ECAM-1 sites/microns2 of plastic surface. B16 melanoma cell binding to Lu-ECAM-1 is blocked by mAb 6D3 and is competitively inhibited by soluble Lu-ECAM-1. C57B1/6 mice passively immunized with anti-Lu-ECAM-1 mAb 6D3 or actively immunized with purified Lu-ECAM-1 exhibit an anti-Lu-ECAM-1 antibody titer-dependent reduction in the number of B16 experimental metastases. Lu-ECAM-1 promotes neither binding nor metastasis of other lung-metastatic tumor cells (e.g., KLN205). Our data indicate that an "antiadhesion" therapy directed at interfering with the adherence of blood-borne tumor cells to organ-specific vascular endothelium is efficient in the control of metastasis formation in selective organ sites.     

丙泊酚对大鼠肠缺血-再灌注后肺细胞间黏附分子-1蛋白表达的影响

目的 研究丙泊酚对大鼠肠缺血-再灌注(I／R)后肺细胞间黏附分子-1(ICAM-1)蛋白表达的 影响。方法 SD大鼠随机分为4组(n=8):①I／R组:暴露腹腔后夹闭肠系膜上动脉(SMA)1 h,开放再灌注 2 h;②丙泊酚预处理组(P1组):肠缺血前10 min给予丙泊酚;③丙泊酚治疗组(P2组):肠再灌注前10 min给 予丙泊酚;④假手术组:仅暴露SMA,不行肠I／R及丙泊酚输注。丙泊酚剂量为首剂10 mg／kg,然后以 10 mg·kg-1·h-1持续输注。所有动物于再灌注2 h处死,检测血浆和肺组织肿瘤坏死因子-α(TNF-α) 及肺组织MPO含量,免疫组化染色检测肺组织ICAM-1蛋白的表达。结果 肠I／R后动物血浆和肺组织 TNF-α含量及肺组织MPO含量、ICAM-1蛋白表达均增加。丙泊酚可以抑制上述改变,以P1组效果最明 显,其中血浆TNF-α及肺组织ICAM-1表达在I／R组和P1组间存在显著性差异(P均<0.05),而P2组上 述各指标显著高于假手术组。结论 ICAM-1在肠I／R后肺损伤的发生中发挥重要作用。肠I／R早期应用丙 泊酚可减少肺组织ICAM-1表达,在一定程度上减轻肺损伤。     

血小板内皮细胞黏附分子-1与百草枯中毒后兔肺损伤的关系

目的 探讨百草枯中毒后肺组织内血小板内皮细胞黏附分子-1(PECAM-1)表达的变化与肺损伤和肺纤维化程度的关系.方法 36只成年新西兰大白兔,依据胃管内灌入百草枯剂量的不同,随机分为8 mg/kg(A组)、16 mg/kg(B组)和32 mg/kg(C组).中毒后观察动物生存状况;7 d后处死动物,取肺组织进行组织学损伤评分、Masson染色鉴定肺纤维化(LF)程度、免疫组化半定量分析PECAM-1的表达,Pearson相关分析法确定PECAM-1表达和ALI、LF程度的关系.结果 每组12只动物,均出现明显的中毒症状,C组存活时间为(6.47±0.99)d,短于B组的(6.09±1.04)d(P=0.031)和A组的(4.77±2.04)d(P=0.007).ALI评分A组为(8.33±1.03),低于B组的(9.83±1.17)(P=0.047)和C组的(11.50±1.38)(P＜0.01),B组与C组相比较,P=0.03.肺纤维化程度A组为(31.09±2.05)%,低于B组的(34.37±1.62)%(P=0.002)和C组的(36.54±0.44)%(P＜0.01),B组和C组之间差异具有统计学意义(P=0.026).A组肺PECAM-1的表达为(20.31±0.70)%,高于B组的(19.34±0.68)%(P=0.16)和C组的(18.37±0.46)%(P＜0.01),B组与C组相比,差异具有统计学意义(P=0.017).Pearson相关分析显示,PECAM-1的表达和ALI评分(Coe=-0.732,P=0.001)、肺纤维化程度(Coe=-0.779,P＜0.001)明显相关.结论 新西兰兔PQ中毒后,肺组织内PECAM-1表达明显下降,成剂量依赖性,与肺损伤程度、肺纤维化程度密切相关;PECAM-1表达的下降在PQ致肺损伤的发生、发展中起重要作用.     

A heterophilic adhesion mechanism for platelet/endothelial cell adhesion molecule 1 (CD31)

The molecular nature of cell adhesion mediated by platelet/endothelial cell adhesion molecule 1 (PECAM-1; CD31) was examined using stably transfected L cells in a PECAM-dependent aggregation assay. This adhesion was temperature sensitive and divalent cation dependent, with Mg2+ supporting aggregation to a greater degree than Ca2+. PECAM-dependent aggregation was heterophilic: PECAM-1 transfectants bound as readily to control-transfected L cells as to other PECAM-1 transfectants, demonstrating that a molecule endogenously expressed on the L cells serves as the ligand for PECAM in this system and presumably substitutes for the natural human ligand.     

急性肺损伤肺大鼠组织细胞间黏附分子表达及生脉饮对其影响

目的 探讨肺组织细胞间黏附分子-1(ICAM-1)表达与急性肺损伤(ALI)的关系以及中药生脉饮对其影响.方法 注射脂多糖(LPS)复制大鼠ALI模型,根据干预因素不同随机分为四组,即生理盐水对照组、LPS组、生脉饮+LPS组、地塞米松+LPS组.观察肺组织病理形态和ALI生物学标志并测定肺组织ICAM-1 mRNA.结果 肺血管内皮细胞ICAM-1 mRNA表达在LPS组显著高于对照组(P<0.01),生脉饮+LPS组和地塞米松+LPS组显著弱于LPS组(P<0.05,P<0.01);肺湿/干质量比,肺泡灌洗液中性粒细胞比、蛋白含量以及肺血管壁通透性、肺泡通透指数也显著小于LPS组.结论 肺组织ICAM-1 mRNA表达增强参与了ALI发生、发展,生脉饮和地塞米松可使肺组织损伤减轻,其机制可能是抑制了肺组织ICAM-1 mRNA表达.     

赛来昔布预处理对大鼠脑缺血再灌注损伤细胞间黏附因子1不同时相点表达的影响

目的:观察赛来昔布预处理对局灶性脑缺血再灌注损伤大鼠的脑梗死体积、脑缺血坏死区周边细胞间黏附分子1不同时相点的影响。方法:实验于2003-12/2004-02在大连医科大学附属第二医院中心实验室进行。SD大鼠36只随机分为3组:赛来昔布组(n=16)、安慰剂组(n=16)及假手术组(n=4),其中赛来昔布组和安慰剂组按脑缺血再灌注2,4,6,24h分为4个亚组(n=4)。手术前10min赛来昔布组用赛来昔布灌胃(0.25mg/g,以3mL生理盐水溶解),安慰剂组安慰剂灌胃,剂量相同,然后制作大脑中动脉闭塞及再通模型,假手术组仅做颈部正中切口暴露右侧颈总动脉后缝合皮肤。观察大鼠大脑中动脉闭塞2h再灌注2,4,6,24h4个时相点梗死体积,并应用免疫组织化学法染色观察细胞间黏附分子1阳性微血管数。结果:36只大鼠进入结果分析。①脑缺血再灌注24h内,安慰剂组随再灌注时间延长,梗死体积逐渐加大;梗死体积最大见于再灌注24h。相同再灌注时间点赛来昔布组梗死体积明显小于安慰剂(t=5.35,4.27,5.21,4.86,P<0.05)。②赛来昔布组及安慰剂组缺血2h再灌注2h后,均可见脑缺血坏死区周边微血管内皮细胞细胞间黏附分子1表达增多,并于24h达高峰;与假手术组比较两组细胞间黏附分子1阳性表达均有明显差异(t=2.25～3.64和2.89～3.58,P<0.01)。相同再灌注时间点赛     

红参附子提取物保护下肾缺血再灌注损伤大鼠细胞间黏附分子1的表达

目的:观察细胞间黏附分子1表达与大鼠肾缺血再灌注损伤的关系及红参附子提取物对其的保护作用。方法:实验于2004-03/2004-09在锦州医学院附属第一医院肾内科实验室完成。将60只雄性SD大鼠以随机数字表法分为3组,即假手术组,模型组,观察组,每组20只。对模型组,观察组大鼠采取右侧肾切除,夹闭左侧肾蒂1h,制造再灌注模型;假手术组仅切除右肾,分离左肾肾蒂但不夹闭。观察组于缺血前0.5h予红参附子提取物(参附注射液,三九雅安制药公司,批号:2003091821,20mL/支)10mL/kg门静脉注射;假手术组和模型组均注射等量生理盐水。各组分别于术后24,48h取10只大鼠处死,取肾脏标本做组织学检查,观察形态学变化,用免疫组化方法检测肾组织中细胞间黏附分子1的表达水平,并计数再灌注模型肾组织中多型核白细胞的浸润数。结果:60只大鼠全部进入结果分析。①模型组镜下可见近曲小管排列紊乱、疏松,有广泛空泡变性及片状坏死,细胞核固缩、深染。远曲小管内有大量管型形成。肾间质局部出血伴炎细胞浸润。观察组肾小管排列基本正常,小管上皮细胞轻度浊肿,偶见管型。炎细胞浸润亦较模型组明显减轻。除假手术组,各组48h改变较24h严重。②模型组肾小管Paller氏评分和肾组织中白细胞计数与假手术组比较,均显著增加(P<0.01),观察组均显著低于模型组(P<0.01)。除假手术组,各组24h与48h间差异有显著性意义(P<0.01)。③假手术组肾脏细胞间黏附分子1仅见微量表达。模型组24h出现明显细胞间黏附分子1表达,48h表达显著高于24h组(P<0.01)。观察组细胞间黏附分子1表达明显弱于模型组(P<0.01)。④再灌注24h及48h肾小管评分与肾组织中白细胞数、细胞间黏附分子1表达均呈正相关(r=0.65,0.58,P<0.05)。肾组织中白细胞数、细胞间黏附分子1表达呈正相关(r=0.85,P<0.05)。结论:细胞间黏附分子1可介导炎细胞浸润并造成肾脏缺血再灌注损伤,红参附子提取物能够抑制这种损伤过程,发挥肾保护作用。     

红参附子提取物保护下肾缺血再灌注损伤大鼠细胞问黏附分子1的表达

目的：观察细胞问黏附分子1表达与大鼠肾缺血再灌注损伤的关系及红参附子提取物对其的保护作用。 方法：实验于2004—03／2004—09在锦州医学院附属第一医院肾内科实验室完成。将60只雄性SD大鼠以随机数字表法分为3组，即假手术组，模型组，观察组，每组20只。对模型组，观察组大鼠采取右侧肾切除，夹闭左侧肾蒂1h，制造再灌注模型；假手术组仅切除右肾，分离左肾肾蒂但不夹闭。观察组于缺血前0.5h予红参附子提取物（参附注射液，三九雅安制药公司，批号：2003091821，20mL／支）10mL／kg门静脉注射；假手术组和模型组均注射等量生理盐水。各组分别于术后24，48h取10只大鼠处死，取肾脏标本做组织学检查，观察形态学变化，用免疫组化方法检测肾组织中细胞间黏附分子1的表达水平，并计数再灌注模型肾组织中多型核白细胞的浸润数。 结果：60只大鼠全部进入结果分析。①模型组镜下可见近曲小管排列紊乱、疏松，有广泛空泡变性及片状坏死，细胞核固缩、深染。远曲小管内有大量管型形成。肾间质局部出血伴炎细胞浸润。观察组肾小管排列基本正常，小管上皮细胞轻度浊肿，偶见管型。炎细胞浸润亦较模型组明显减轻。除假手术组，各组48h改变较24h严重。②模型组肾小管Paller氏评分和肾组织中自细胞计数与假手术组比较，均显著增加（P＜0．01），观察组均显著低于模型组（P＜0．01）。除假手术组，各组24h与48h间差异有显著性意义（P＜0．01）。③假手术组肾脏细胞间黏附分子1仅见微量表达。模型组24h出现明显细胞间黏附分子1表达，48h表达显著高于24h组（P＜0．01）。观察组细胞间黏附分子1表达明显弱于模型组（P＜0．01）。④再灌注24h及48h肾小管评分与肾组织中自细胞数、细胞间黏附分子1表达均呈正相关（r=0．65，0．58，P＜0．05）。肾组织中自细胞数、细胞间黏附分子1表达呈正相关（r=0．85，P＜0．05）。 结论：细胞间黏附分子1可介导炎细胞浸润并造成肾脏缺血再灌注损伤，红参附子提取物能够抑制这种损伤过程，发挥肾保护作用。     

丹参酮对脑梗死患者白细胞表面黏附分子表达的影响

目的:通过对白细胞表面黏附分子表达的分析,探讨丹参酮治疗急性脑梗死的作用机制。方法:采用双盲随机对照方法将80例急性脑梗死患者分为两组,治疗组给予丹参酮注射液2 m l,对照组给予注射用水,两组分别溶于生理盐水250 m l静脉滴注,每日1次,连用7 d。两组于治疗前后取外周血分离多形核白细胞(PM N),应用间接免疫荧光标记,流式细胞仪检测白细胞表面黏附分子CD 11a、CD 18、CD 18/CD 11a(LFA 1)免疫阳性细胞数;应用透射电镜观察外周血PM N超微结构变化。结果:丹参酮能明显降低外周血白细胞表面黏附分子CD 11a、CD 18、LFA 1免疫阳性细胞数;PM N超微结构显示,与治疗组比较,对照组胞浆电子密度降低,内质网扩大,部分线粒体嵴断裂,核周间隙增高,核浆比例增大均更加明显。结论:丹参酮抑制白细胞表面黏附分子CD 11a、CD 18、LFA 1的表达,阻断白细胞与血管内皮细胞黏附,在脑梗死治疗中具有保护神经细胞的作用。     

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(英文)

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.