慢性静脉功能不全粘附分子CD11b/CD18、ICAM-1表达及意义

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

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。

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-CDllb plsitively expression increased remarkably in class 2-3 compared with that in class 1 and contrast group.The index of PMN-CD 18 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 CD1 1b/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 α and IL-1β , to upregulate ICAM-1 and CD1 1b/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.