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目的探讨细胞间粘附分子（ＩＣＡＭ－１）是否介导缺氧－再氧化引起的中性粒细胞（ＰＭＮ）和血管内皮细胞（ＶＥＣ）的粘附反应。方法血管内皮细胞（ＶＥＣ）经缺氧再氧化（Ｈ／Ｒ）处理后，加入ＰＭＮ，用计数法检测粘附率，以细胞免疫化学及原位杂交法检测ＩＣＡＭ－１及ＩＣＡＭ－１ｍＲＮＡ表达。结果ＶＥＣ经Ｈ／Ｒ处理后，ＰＭＮ与其粘附率增高１倍（Ｐ＜０．０１），ＩＣＡＭ－１单克隆抗体（ｍＡｂ）与ＣＤ１１ａ／ＣＤ１８ｍＡｂ可明显降低粘附率的增高，Ｈ／Ｒ能增加ＶＥＣ的ＩＣＡＭ－１及ＩＣＡＭ－１ｍＲＮＡ表达。结论ＩＣＡＭ－１介导Ｈ／Ｒ后的ＰＭＮ－ＶＥＣ间粘附反应。
Objective To investigate whether intercellular adhesion molecule (ICAM-1) mediates the adhesion of neutrophils (PMN) and vascular endothelial cells (VEC) induced by hypoxia-reoxygenation. Methods The vascular endothelial cells (VECs) were treated with hypoxia and reoxygenation (H / R), PMN was added and the adhesion rate was measured by counting method. The expressions of ICAM-1 and ICAM-1 mRNA were detected by immunocytochemistry and in situ hybridization. Results The adhesion rate of PMN to VEC was increased by 1 time (P <0.01) by H / R treatment. ICAM-1 monoclonal antibody (mAb) and CD11a / CD18 mAb could significantly reduce the adhesion rate. Can increase the ICAM-1 and ICAM-1 mRNA expression of VEC. Conclusion ICAM-1 mediates PMN-VEC adhesion after H / R.