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目的：探讨抗巨噬细胞活化趋化因子１（Ｍａｃ１）抗体保护神经元缺血性损伤的作用机制。方法：２４只Ｗｉｓｔａｒ大鼠随机分为４组：正常对照组（４只）、伪手术组（４只）、脑缺血再灌注损伤组（脑缺血组，８只）、脑缺血再灌注损伤加Ｍａｃ１抗体实验组（脑缺血加抗体组，８只）。分离培养鼠脑毛细血管内皮细胞（ＣＣＥＣ）和多形核白细胞（ＰＭＮ），利用微管吸吮技术，观察ＰＭＮ与ＣＣＥＣ间粘附力学特性的变化。结果：脑缺血再灌注后各时间点，ＰＭＮ与ＣＣＥＣ粘附力和粘附应力均明显高于正常对照组和伪手术组（Ｐ均＜０．０１）；加抗Ｍａｃ１抗体后，细胞粘附力和粘附应力均明显下降（Ｐ＜０．０５或Ｐ＜０．０１）。结论：脑缺血再灌注损伤后抗Ｍａｃ１抗体使ＰＭＮ与ＣＣＥＣ粘附力减小，粘附应力下降；抗粘附分子抗体将可能成为治疗缺血性脑血管疾病的一条新的有效途径
Objective: To investigate the mechanism of anti-macrophage-derived chemokine 1 (Mac1) antibody in protecting neuron against ischemic injury. Methods: Twenty-four Wistar rats were randomly divided into four groups: normal control group (n = 4), sham operation group (n = 4), cerebral ischemia-reperfusion injury group Perfusion injury plus Mac1 antibody experimental group (cerebral ischemia and antibody group, 8). The cultured rat brain capillary endothelial cells (CCECs) and polymorphonuclear leukocytes (PMNs) were isolated and cultured. The changes of adhesion mechanics between PMN and CCEC were observed by microtubule sucking technique. Results: The adhesion and adhesion stress of PMN and CCEC at each time point after cerebral ischemia-reperfusion were significantly higher than those in normal control group and sham operation group (all P <0.01). After anti-Mac1 antibody was added, Adhesion and adhesion stress were significantly decreased (P <0.05 or P <0.01). CONCLUSION: Anti-Mac1 antibody reduces the adhesion between PMN and CCEC after cerebral ischemia-reperfusion injury, and the adhesive stress decreases. Anti-adhesion molecule antibodies may be a new and effective approach for the treatment of ischemic cerebrovascular disease