Expression of adnesion molecules ICAM-1.CD11b/CD18 in chronic venous insufficiency and their clinical implication

Zhou Xiaohong; et al

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Expression of adnesion molecules ICAM-1.CD11b/CD18 in chronic venous insufficiency and their clinical implication

更新时间：2024-01-17

- Expression of adnesion molecules ICAM-1.CD11b/CD18 in chronic venous insufficiency and their clinical implication
- Journal of Chongqing Medical University Issue 5, Pages: 701-703(2006)
- 作者机构：
  
  1. 重庆市璧山县人民医院外科
  2. 重庆市第八人民医院
- 作者简介：
- 基金信息：
- DOI：
  CLC： R654.3
- Published：2006，
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[1]周晓宏,乔正荣,梁栋.慢性静脉功能不全粘附分子CD11b/CD18、ICAM-1表达及意义[J].重庆医科大学学报,2006(05):701-703+717.

Zhou Xiaohong, et al. Expression of adnesion molecules ICAM-1.CD11b/CD18 in chronic venous insufficiency and their clinical implication. [J]. Journal of Chongqing Medical University (5):701-703(2006)
[1]周晓宏,乔正荣,梁栋.慢性静脉功能不全粘附分子CD11b/CD18、ICAM-1表达及意义[J].重庆医科大学学报,2006(05):701-703+717. DOI：

Zhou Xiaohong, et al. Expression of adnesion molecules ICAM-1.CD11b/CD18 in chronic venous insufficiency and their clinical implication. [J]. Journal of Chongqing Medical University (5):701-703(2006) DOI：

摘要

目的:探讨CVI粘附分子表达与皮肤损伤的关系。方法:采用ELISA法

免疫组织化学法（SP法）和电镜超微结构研究32例CVI患者和8例正常对照组。结果:①class2￣3级EC-ICAM-1和PMN-CD11b阳性表达率显著高于class1级和对照组（P<0.05）

class2￣3级和class1级PMN-CD18阳性表达率明显高于对照组（P<0.05）;②相关分析显著

ICAM-1表达与CD11b和CD18表达呈显著正相关;③电镜超微结构证明;PMN与Ecs粘附导致皮肤微血管病变。结论:CVI血浆TNFα、IL-1β增高

上调ICAM-1和CD11b/CD18表达

并介导PMN粘附于ECs

导致ECs和组织损伤

可能是静脉溃疡重要的发病机制之一。

Abstract

Objective:Explore the relationship between AMS expression and skin damage.Metheds:The study employed ELISA method

immunohistochemical method and electron minroscope analysis.Results:The results showed that the index of EC-ICAM-1 and PMN-CD11b plsitively expression increased remarkably in class 2~3 compared with that in class 1 and contrast group.The index of PMN-CD18 expression in class 2~3 and class 1 was greatly higher than that in contrast groups(P <0.05).The expression of ICAM-1 was positively correlated with that of CD11b/CD18.Electron microcopy showed that the change microvessel was mainly PMN adhesion with ECs and trapped in microvessels.Conclusions:It was suggested that activated monocyte to release TNF αand IL-1β

to upregulate ICAM-1 and CD11b/CD18

to mediate PMN adhesion with Ecs

and to cause Ecs and skin tissue damage.It may be one of important mechanism of venous ulcer.

关键词

粘附分子ICAM-1CD11b/CD18静脉功能不全

Keywords

Adhesion moleculesICAM-1CD11b/CD18Venous insufficiency

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