Pingyangmycin-regulated expressions of adhesion molecules in human venous malformation endothelial cells

Pingyangmycin (bleomycin A5 hydrochloride,PYM) is one of the anti-neoplastic agents which have been commonly used to treat venous malformations.However,the underlying mechanism by which PYM treats venous malformations remains poorly understood.It was reported that venous endothelial cells could recruit neutrophils via adhesion molecules (E-selectin,ICAM-1,ICAM-3,VCAM-1) during the acute/chronic inflammation and subsequent histological fibrosis after sclerotherapy with PYM.This study explored if the expression of E-selectin,ICAM-1,ICAM-3 and VCAM-1 in human venous malformation endothelial cells could be affected by PYM.HVMECs were cultured from human venous malformation tissue.Expressions of E-selectin,ICAM-1,ICAM-3 and VCAM-1 on HVMECs in response to PYM were analyzed by cell ELISA.The relative levels of mRNA expression in the cells were semi-quantified.The results showed that PYM up-regulated the expressions of E-selectin,ICAM-3,VCAM-1 and ICAM-1 in both time-and concentration-dependent manner.Our findings suggested that PYM could induce the expression of adhesion molecules in HVMECs,which might be a possible mechanism by which sclerotherapy by intralesional injection of PYM treats venous malformations.     

细胞间黏附分子1和血管细胞黏附分子1在血管瘤组织中表达的意义

目的：探讨细胞间黏附分子1（ICAM-1）和血管细胞黏附分子1（VCAM-1）在小儿血管瘤增殖退化病理生理演变过程中的表达及作用机制.方法：应用SABC免疫组化法检测28例增殖期血管瘤及22例退化期血管瘤的ICAM-1、VCAM-1在血管内皮细胞上的表达情况,同时以血管畸形及正常皮肤为对照.结果：ICAM-1在增殖期血管瘤强阳性表达,退化期阳性表达,两时期差异十分显著（P＜0.01）;VCAM-1在增殖期和退化期血管瘤均为阳性表达,两时期无明显差异;ICAM-1和VCAM-1在血管畸形和正常皮肤几乎均为阴性表达,与不同时期血管瘤相比差异均十分显著（P＜0.01）.结论：ICAM-1可能在血管形成早期发挥作用,介导内皮细胞间黏附,参与血管瘤发病和消退的病理过程.     

芪丹通脉片对实验性动脉粥样硬化大鼠动脉壁ICAM-1、VCAM-1基因表达的影响

目的: 观察芪丹通脉片(QDTMT)对实验性动脉粥样硬化(AS)大鼠动脉壁匀浆中细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)表达的影响,探讨QDTMT的抗AS机制. 方法: 将健康雄性SD大鼠72只按体质量随机分为6组,每组12只:模型组(model)、空白对照组(control)、阳性对照辛伐他汀组(simvastatin)、QDTMT低剂量组(QDTMTL)、QDTMT中剂量组(QDTMTM)、QDTMT高剂量组(QDTMTH). 采用高脂饮食配合口服维生素D3建立大鼠AS模型,各组动物ig给药. 采用半定量RT-PCR的方法检测各组动物动脉壁匀浆中ICAM-1和VCAM-1基因的表达,分析造模及各药物组ICAM-1和VCAM-1基因表达的变化. 结果: 与空白对照组相比,模型组ICAM-1和VCAM-1基因的表达明显增加(P<0.01);与模型组相比,辛伐他汀组及各中药组均能减少ICAM-1和VCAM-1基因的表达(P<0.01-0.05),且QDTMTH的作用明显优于QDTMTL(P<0.05). 结论: QDTMT能下调实验性AS大鼠动脉壁ICAM-1和VCAM-1基因的表达,这可能是QDTMT抗AS的机制之一.     

细胞间黏附分子-1与血管细胞间黏附分子-1在血管慢性排斥反应中的表达及霉酚酸酯的抑制作用

目的探讨大鼠同种异体腹主动脉移植慢性排斥反应期间移植动脉细胞间黏附分子-1（ICAM-1）及血管细胞黏附分子-1（VCAM-1）的表达及霉酚酸酯（MMF）对移植动脉排斥反应的抑制作用。方法建立大鼠腹主动脉移植模型,设Wistar到Wistar大鼠的同系腹主动脉移植对照组、SD大鼠到Wistar大鼠的同种移植组、同种移植MMF治疗组和抗黏附分子单克隆抗体治疗组。采集移植动脉组织标本行免疫组织化学和组织病理学检查,对移植动脉组织ICAM-1及VCAM-1的表达进行定量检测。结果对照组移植动脉组织ICAM-1、VCAM-1表达较弱;同种移植组在排斥反应期间移植动脉组织血管内皮细胞的ICAM-1、VCAM-1表达强度和数量明显增加,且伴有大量淋巴细胞浸润;MMF治疗组移植动脉仅微弱表达ICAM-1、VCAM-1,同时少有淋巴细胞浸润,与黏附分子单克隆抗体治疗相似。结论ICAM-1、VCAM-1的表达水平与慢性排斥反应的发生和发展有关;MMF能显著抑制移植肾ICAM-1和VCAM-1的表达和淋巴细胞的浸润,明显延长移植物的存活。     

克罗恩病患者血浆中细胞间黏附分子-1和血管细胞黏附分子-1水平检测的临床意义

检测96例克罗恩病( CD)患者和48例正常对照者血浆细胞黏附分子-1 ( ICAM-1 )和血管细胞黏附分子( VCAM-1)水平,与对照组比较,CD组血浆中ICAM-1和VCAM-1水平均明显增高(P<0. 01). 按疾病严重程度分组,各组血浆中ICAM-1和VCAM-1水平比较差异均有统计学意义( P<0. 01);按临床特征分组,各组内血浆中ICAM-1 和VCAM-1水平比较差异均无统计学意义. CD患者血浆中ICAM-1和VCAM-1水平明显增高,与疾病严重程度有一定关联,与临床特征无明显关联.     

脑梗死患者血清中IL-1和sICAM-1、sVCAM-1变化的研究

目的　了解脑梗死患者血清中IL 1和sICAM 1、sVCAM 1含量变化及意义。方法　用双抗体夹心酶联免疫吸附法测定血清中IL 1、sICAM 1、sVCAM 1的含量。结果　急性期脑梗死患者血清IL 1、sICAM 1、sVCAM 1的水平显著高于其他各组 ,差异有显著性 (P <0 0 1或P <0 0 5 ) ,且sICAM 1、sVCAM 1均与IL 1呈正相关 (r =0 4 9,P <0 0 1;r =0 6 5 ,P <0 0 0 1) ;结论　sICAM 1、sVCAM 1可能参与了临床缺血性脑损伤的病理过程。sICAM 1、sVCAM 1水平的增高可能与IL 1有关 ,临床脑缺血后粘附分子表达上调可能与炎性细胞因子IL 1有关。     

登革病毒感染对人血管内皮细胞血管细胞黏附分子-1表达的影响

目的:研究登革病毒2型(DV2)体外感染对人脐静脉内皮细胞(HUVEC)表达血管细胞黏附分子-1(VCAM-1)的影响.方法:原代分离、纯化、培养人HUVEC细胞,用生长良好的2～3代细胞进行实验.分别用病毒感染复数(MOI)为1、2、4、8、16的DV2病毒液感染HUVEC,阴性对照组直接以RPMI 1640培养,应用细胞计数试剂-8(CCK-8)法测定DV2感染前和感染后6、12、24、48、72和96 h的细胞活性.另以MOI=2的DV2病毒液感染细胞,阴性对照组直接以RPMI 1640培养,于感染后6、12、24、48、72、96 h分别收集病毒感染的HUVEC,采用流式细胞术测定细胞表面VCAM-1表达水平;采用RT-PCR法检测细胞中VCAM-1 mRNA转录水平.结果:当病毒MOI=2时对细胞活力的影响与对照组相比差异无统计学意义.DV2感染可以促进HUVECs中VCAM-1 mRNA的转录,96 h内均有增加,与对照组相比有显著性差异(P<0.05).其中,正常状态下HUVEC基本无VCAM-1 mRNA转录,感染12 h达到最高峰,12～48 h表达量显著高于其他时间(P<0.05).DV2 感染HUVEC后, VCAM-1蛋白表达在12～72 h显著升高(P<0.05),与对照组相比差异有统计学意义(P<0.05).结论:DV2感染上调HUVEC的VCAM-1 mRNA转录和蛋白表达.这可能是DV2感染诱发患者血管通透性升高和血浆渗漏的重要分子机制之一.     

雷公藤红素阻断全反式维甲酸导致的白血病细胞与内皮细胞黏附

目的:全反式维甲酸(all-trans retinoic acid,ATRA)治疗急性早幼粒细胞白血病,引起白血病细胞与内皮细胞之间黏附增加,是发生维甲酸综合征的重要原因。本文观察雷公藤红素对这种黏附增加的影响。方法:用流式细胞术检测雷公藤红素对急性早幼粒细胞白血病细胞系NB4和人脐静脉内皮细胞(humanumbilical vascular endothelial cell,HUVEC)在ATRA刺激下表达黏附分子的影响。用细胞黏附功能实验,检测雷公藤红素对ATRA导致的上述两种细胞之间黏附增加的影响。结果:ATRA能引起NB4细胞表面细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)表达增加,但可被雷公藤红素明显抑制(P<0.01)。NB4细胞上清液能刺激HUVEC表达ICAM-1(P<0.05);而被ATRA处理过的NB4细胞上清液能明显刺激HUVEC表达选择素E(E-selectin)、血管细胞黏附分子-1(vascular cell adhesion molecule-1,VCAM-1)和ICAM-1等黏附分子(P<0.01),雷公藤红素对其抑制率分别达25.3%、42.4%和61.0%。ATRA导致上述两种细胞之间黏附增加,雷公藤红素对其完全抑制。结论:雷公藤红素能抑制ATRA导致的白血病细胞与内皮细胞黏附,有可能用于维甲酸综合征的治疗。     

Dynamic Expression of Tumor Necrosis Factor-α and Vascular Endothelial Growth Factor in Rat Model of Pulmonary Emphysema Induced by Smoke Exposure

In order to explore the roles of tumor necrosis factor-α(TNF-α) and vascular endothelial growth factor(VEGF) in the pathogenesis of pulmonary emphysema,male Wistar rats were randomized into group A1,group A2.5 and group A4,each with smoke exposure for 1 month,2.5 months or 4 months,respectively.Group B1,group B2.5 and group B4 were used as non smoking controls at corresponding time points.TNF-α in bronchoalveolar lavage fluid(BALF) and expression of VEGF in lung tissue was determined by ELISA or by SABC immunohistochemistry assay either.Lung slices were stained with hematoxylin and eosin(HE).Results showed that in animal with smoke exposure the mean linear interceptor(Lm),an index of pulmonary emphysema and the content of TNF-α in BALF increased gradually,on contrary,the expression of VEGF in lung tissue decreased(P<0.05).This phenomenon was not obvious in animals without smoke exposure.Lm was negatively correlated to the VEGF expression(γ=-0.81,P<0.01) and positively correlated to TNF-α concentration(γ = 0.52,P<0.004),which implies that smoke exposure decreased the expression of VEGF and increased the expression of TNF-α.It is plausible to speculate that the imbalance of TNF-α and VEGF may play an important role in the pathogenesis of smoke-induced pulmonary emphysema.     

急性缺血性脑血管病患者血清IL-1、TNF-α和sVCAM-1动态变化及临床意义

目的　探讨脑缺血患者血清白细胞介素 -1(IL -1)、肿瘤坏死因子 -α(TNF -α)和可溶性血管细胞间粘附分子 -1(sVCAM)水平的动态变化规律及其意义。方法　应用ELISA法分别检测脑缺血后第 1、2、5天患者血清中IL -1、TNF -α、sVCAM -1水平。结果　发病后 2 4小时内患者血清中IL -1、TNF -α、sVCAM -1水平即开始升高 ,分别为 0 .3 8± 0 .16ng/ml、1.63± 0 .61ng/ml、687.19± 3 5 6.76ng/ml。其中IL -1、TNF -α血清浓度于 2 4小时内达到最高峰 ,第二天有所下降 0 .2 5± 0 .12ng/ml、1.40± 0 .71ng/ml,第五天下降至接近正常水平 0 .18± 0 .0 9ng/ml、0 .73± 0 .3 2ng/ml。sVCAM -1血清浓度于发病后第二天达到高峰 990 .79± 3 68.3 6ng/ml,第五天有所下降但仍维持在较高水平 977.70± 3 84.16ng/ml。发病后第二天IL -1水平与sVCAM -1水平升高呈线性正相关。结论　脑缺血患者血清IL -1、TNF -α、sVCAM -1水平均升高 ,表明IL -1、TNF -α和sVCAM -1可能参与了脑缺血损伤过程     

血透患者可溶性细胞粘附分子的变化

目的 探讨血透对可溶性细胞粘附分子表达的影响。方法 观察２２例尿素症血透患者透析前、透析１５分钟及透析５小时后血中可溶性ｓＩＣＡＭ－１和血浆Ｐ－选择素的水平,同时相应进行白血细胞计数。结果 患者透析１５分钟钟的血白细胞显著低于透析前水平,透析５小时后接近透析前水平,两者差异无显著性。透析前ｓＩＣＡＭ－１水平高于正常对照组,透析１５分钟时静脉端显著低于透析前水平,但高于动脉端水平,透析５小时后其值仍     

可溶性细胞粘附分子与动脉粥样硬化不稳定斑块关系的研究

目的　探讨急性冠脉综合征患者血清中可溶性粘附分子的水平与冠状动脉不稳定斑块的关系。方法　应用酶联免疫吸附法 (ELISA)检测 3 1例急性冠脉综合征 (ACS) (其中不稳定性心绞痛 19例 ,急性心肌梗塞 12例 )和 12例稳定性心绞痛患者及 10例正常对照组血清中可溶性血管细胞粘附分子 -1(sVCAM -1)和可溶性细胞间粘附分子 -1(sICAM -1)的水平。结果　不稳定性心绞痛、急性心肌梗塞及稳定性心绞痛血清中sVCAM -1和sICAM -1水平比对照组明显增高 ,与稳定性心绞痛相比 ,不稳定性心绞痛患者血中的sVCAM -1和sICAM -1水平明显增高 (P均 <0 .0 1) ,急性心肌梗塞患者血清中水平较不稳定性心绞痛明显增高 (P <0 .0 1)。结论　通过检测急性冠脉综合征患者血清中sVCAM -1和sICAM -1水平 ,可预测其病情和预后 ,操作方法简便。     

急性冠状动脉综合征患者血清sICAM-1、sVCAM-1表达与可溶性P-选择素关系的研究

目的：观察急性冠脉综合征（ACS）患者血清中可溶性细胞间黏附分子-1（sICAM-1）、血管细胞黏附分子-1（sVCAM-1）及P选择素（sP—selectin）水平的变化。方法：选择稳定型心绞痛患者（SAP组）30例、不稳定型心绞痛患者（uA组）30例、急性心肌梗死患者（AMI组）25例,采用ELISA法检测其外周血血清可溶性P选择素、sICAM-1和sVCAM-1水平。以健康体检者30例作为对照。结果：ACS组血清sICAM-1、sVCAM-1、sP—selectin水平显著高于SAP组和对照组（均P〈0．01）,SAP组与对照组无显著性差异（P〉0．05）。ACS患者血清sICAM-1、sVCAM-1与sP—selectin呈显著正相关（r=0．519,0．517,均P〈0．05）。结论：ACS患者血清sICAM-1、sVCAM-1和sP—selectin水平均明显升高,它们共同作用促进ACS的发生和发展。     

Levels of soluble adhesion molecules in patients with various clinical presentations of coronary atherosclerosis

Background Adhesion molecules play an important role in the development and progression of coronary atherosclerosis. The aim of this study was to compare concentrations of soluble forms of adhesion molecules in patients with different clinical presentations of coronary artery disease （CAD）.Methods One hundred and twenty-eight patients with CAD were divided into three groups; the first group was acute myocardial infarction group （AMI group, n=45）, the second group was unstable angina pectoris group （UAP group, n=48）,the third group was stable angina pectoris group （SAP group, n=35）. We compared them with patients with normal coronary arteries （control group, n=31）. The serum levels of vascular cell adhesion molecule （VCAM-1）, intercellular adhesion molecule-1 （ICAM-1）, E-selectin and P-selectin were measured in all subjects.Results The serum level of VCAM-1 in the AMI group was significantly higher than in the UAP, SAP and control groups （P 〈0.01）. The level in the UAP group was significantly higher than the SAP group and control group （P 〈0.01） and the level in the SAP group was significantly higher than in the control group （P 〈0.01）. The serum ICAM-1 level was significantly elevated in the AMI, UAP and SAP groups as compared to the control group （P 〈0.01）. The levels of serum E-selectin and P-selectin in the AMI and UAP groups were significantly higher than in the SAP and control groups （P〈0.01）.Conclusions Increased levels of VCAM-1 and ICAM-1, E-selectin and P-selectin, as markers of inflammation, showed the importance of inflammatory processes in the development of atherosclerosis and clinical expression of CAD. Soluble ICAM-1, VCAM-1, E-selectin and P-selectin concentrations are useful indicators of the presence of atherosclerosis and the severity of CAD clinical presentation.     

Interleukin-1β, tumor necrosis factor-α and lipopolysaccharide induce expression of monocyte chemoattractant protein-1 in calf aortic smooth muscle cells

Summary To investigate whether interleukin-1β(IL-1β), tumor necrosis factor-α (TNF-α) and lipopolysaccharide (LPS) induce expression of monocyte chemoattractant protein-1 (MCP-1) mRNA and protein in calf aortic smooth muscle cells (SMCs), calf aortic SMCs were cultured by a substrate-attached expiant method. The cultured SMCs were used between the third to the fifth passage. After the cells became confluent, the SMCs were exposed to 2 ng/ml IL- 1β, 20 ng/ml TNF-1α and 100 ng/ml LPS respectively, and the total RNA of SMCs which were incubated for 4 h at 37 C were extracted from the cells by using guanidinium isothiocyanate method. The expression of MCP-1 mRNA in SMCs was detected by using dot blotting analysis using a probe of γ-³²P-end-labelled 35-mer oligonucleotide. After a 24-h incubation, the media conditioned by the cultured SMCs were collected. The MCP-1 protein content in the conditioned media was determined by using sandwich ELISA. The results were as follows: Dot blotting analysis showed that the cultured SMCs could express MCP-1 mRNA. After a 4-h exposure to IL-1β, TNF-α and LPS, the MCP-1 mRNA expression in SMCs was increased (3.6-fold, 2.3-fold and 1.6-fold, respectively). ELISA showed that the levels of MCP-1 protein in the conditioned media were also increased (2. 9-fold, 1.7-fold and 1.1-fold, respectively). The results suggest that calf aortic SMCs could express MCP-1 mRNA and protein. IL-1β and TNF-α can induce strong expression of MCP- 1 mRNA and protein, and the former is more effective than the latter. This project was supported by a grant from National Natural Science Foundation of China (No. 39470289).     

急性缺血性脑血管病患者血清sICAM-1和sVCAM-1动态变化及临床意义

目的 :探讨脑缺血患者血清可溶性细胞间粘附分子 1(sICAM 1)和可溶性血管细胞间粘附分子 1(sVCAM 1)水平的动态变化规律及其意义。方法 :应用ELISA法分别检测脑缺血后第 1、2、5天患者血清中sICAM 1、sVCAM 1水平 ,同时测定第 2天血糖水平。结果 :发病后 2 4小时内患者血清中sICAM 1、sVCAM 1水平即开始升高 ,分别为 2 6 6 .2 8± 6 2 .16ng/ml、6 87.19±356 .76ng/ml;第 2天明显升高 2 85.77± 6 8.4 3ng/ml、990 .79± 36 8.36ng/ml;第 5天又有所下降 ,分别为 2 6 3.6 0± 87.82ng/ml、977.70± 384 .16ng/ml,但仍高于对照组。发病后第 2天血糖水平与sICAM 1水平升高呈线性正相关。结论 :脑缺血患者血清sICAM 1、sVCAM 1水平均升高 ,表明ICAM 1和VCAM 1可能参与了脑缺血损伤过程     

层流状态下高、低切应力对动脉重构及血管细胞粘附分子-1表达的影响

目的制备小鼠腹主动脉狭窄模型,探讨近似层流状态下高、低切应力对动脉重构及VCAM-1表达的影响。方法 20只小鼠随机平均分为狭窄1 d组、7 d组、14 d组和假手术对照组,用动脉银夹建立腹主动脉局部狭窄模型,超声检测狭窄近心端和狭窄处血流动力学参数,计算切应力值;血管标本行HE染色和内皮血管细胞粘附分子-1(VCAM-1)免疫组织化学染色,定量分析动脉病理结构的改变及内皮VCAM-1表达的强度。结果狭窄动脉近心端和狭窄处分别形成低、高切应力血流区,与对照组比较,随着作用时间的增加,狭窄近心端动脉内中膜逐渐增厚、内皮VCAM-1表达逐渐增强,而狭窄处动脉无明显结构改变及内皮VCAM-1表达。结论血流动力学改变,尤其是低切应力可较早引起动脉重构,可能通过内皮VCAM-1的介导作用导致动脉粥样硬化的发生、发展,而高切应力则可能有抗动脉粥样硬化作用。     

哮喘患者血清可溶性E选择素、血管细胞黏附分子1浓度的变化

目的测定哮喘患者循环中可溶性血管细胞黏附分子1(sVCAM-1)及可溶性E选择素(sE-selectin)浓度,并探讨可溶性细胞黏附分子的变化在哮喘发病中的意义.方法38例非发作期哮喘患者的循环中sVCAM-1和sE-selectin测定采用酶联免疫吸附法(ELISA).38例患者包括重度哮喘12例,轻、中度哮喘26例.结果血清中sVCAM-1和sE-selectin浓度较正常对照组显著提高(P＜0.01,P＜0.05);重症哮喘患者sVCAM-1和sE-selectin水平均较正常对照和轻、中度哮喘患者增高非常显著.重症哮喘患者的血清sVCAM-1和sE-selectin测定值之间具有显著相关性(r=0.49,P＜0.05).结论哮喘患者可溶性细胞黏附分子水平sVCAM-1和sE-selectin显著提高,并可能与哮喘的严重性相关,这些分子有可能成为哮喘炎症严重程度和血管内皮细胞损伤或活化的标志.     

胍丁胺抑制单核-内皮细胞黏附作用及其机制的研究

目的探讨内源性胍丁胺对氧化低密度脂蛋白（oxidized low density lipoprotein,ox-LDL）诱导的单核-内皮细胞黏附的作用及其可能的机制。方法体外培养人脐静脉内皮细胞（human umbilical vein endothelial cells,HUVEC）,用不同浓度的胍丁胺作用于ox-LDL诱导的HUVEC 24h,加或不加硝基精氨酸甲酯（L-NAME）,观察人单核细胞对HUVEC的黏附及ICAM-1在HUVEC的蛋白表达。结果胍丁胺浓度依赖地抑制ox-LDL诱导的单核细胞对HUVEC的黏附及ICAM-1在HUVEC的表达（P〈0．01）,二者成正相关（r=0．8857,P〈0．001）,加入L-NAME后AGM的作用减弱（P〈0．05）。结论AGM可能通过下调ICAM-1的表达抑制循环单核细胞与内皮细胞的黏附,该作用与一氧化氮合酶（NOS）有关。     

急性冠脉综合征患者细胞黏附分子和C反应蛋白的变化

目的：检测急性冠脉综合征（ACS）患者血清中血管细胞黏附分子（VCAM-1）、细胞间黏附分子（ICAM-1）及C反应蛋白（CRP）水平,探讨其变化在冠心病（CHD）发病及诊断中的意义。方法：检测50例经冠脉造影证实为ACS患者血清中VCAM-1、ICAM-1和CRP的水平,以50例经冠脉造影正常者作对照。结果：ACS患者血清中VACM-1、ICAM-1和CRP水平明显高于对照组,分别为(701±54.6)和(556±42.2)μg·L^-1（P<0.01）、(389±23.7)和(271±34.6)μg·L^-1（P<0.01）及(7.05±3.13)和(4.22±1.41)mg·L^-1（P<0.01）;急性心肌梗塞（AMI）与不稳定心绞痛（UA）患者VCAM-1和ICAM-1无统计学差异［（699.12±62.77)和(706.57±53.65)、(390.39±42.34)和(372.63±32.59μg·L^-1］(P>0.05);AMI患者CRP含量明显高于UA 患者［（8.06±2.78)和(6.33±2.01)mg·L^-1］(P<0.05)。结论：动脉粥样斑块所致的动脉狭窄和闭塞病变伴随着介导血管炎症的VCAM-1、ICAM-1及CRP水平的增高,并且与病变严重程度相关,其过度表达可能是动脉粥样硬化（AS）发生的重要因素之一,有望成为动脉粥样硬化发生发展和病情监测指标。