ICAM-1在大鼠肠粘膜屏障损伤中的作用

Effects of ICAM-1 on intestinal mucosal barrier dysfunction in rats with ischemia-reperfusion injury

目的:探讨ICAM-1在大鼠肠缺血再灌注(I/R)过程中对肠粘膜屏障损伤的作用。方法:采用大鼠肠系膜上动脉(SMA)夹闭1小时后松夹造成缺血再灌注损伤动物模型。将42只SD大鼠随机分为造模组、对照组和治疗组。分别于缺血即刻、1小时和再灌注1小时3个时相应用免疫组织化学的方法观察小肠ICAM-1表达,同时检测组织髓过氧化物酶和血浆二胺氧化酶活性、门静脉血细菌培养等指标。结果:ICAM-1蛋白表达在对照组肠缺血1小时及再灌注1小时组较造模组、治疗组增多(P<0.05),组织髓过氧化物酶活性、血浆二胺氧化酶活性升高(P<0.05)。结论:肠缺血再灌注时肠血管内皮细胞ICAM-1表达增加,由此介导的中性粒细胞在局部聚集、活化可能是肠粘膜屏障损伤的病理生理学基础。

objective： To investigate the effect of ICAM-1 on rat intestinal ischemia-reperfusion injury. Methods： Rat intestinal I/ R injury produced by occlusion of the superior mesenteric artery （SMA） for 60 minutes followed by reperfusion used as an animal model. 42 SD rats were randomly divided into the sham-operation group, the ischemia-reperfusion group and the treated group. Tissue samples were taken at the beginning, lh after ischemia, and lh after reperfusion in three groups respectively. The expression of ICAM- 1 in the gut was assayed with immunohistochemistry. Myeloperoxidase （MPO） activity was determined as well. Rescult： The ICAM-1 protein highly express at lh post-ischemia and lh reperfusion; MPO and DAO activities were enhanced（P〈0.05） in accordance with I- CAM-1 in the ischemia-reperfusion group as compared with those in the sham-operation group and the treated group （P〈0.05）. Conclusions： The aggregation and activation of PMN in intestine tissue are associatesd with the high expression of ICAM-1 on intestinal vascular endothelial cells in gut ischemia-reperfusion rats,which might be the mechanisms underlying intestinal mucosa injury and enhanced intstinal permeability.