红细胞诱导的粥样斑块炎症中NF-κB涉及的机制研究

Mechanisms involving NF-κB of erythrocyte-induced inflammation in atherosclerotic plaques

目的了解斑块内出血后红细胞诱导的斑块炎症反应并探讨其中NF-κB涉及的机制。方法取新西兰大白兔28只,球囊拉伤腹主动脉建立动脉粥样硬化模型。通过血管内超声(IVUS)在每只动物的腹主动脉上选定3个厚度相近的斑块,其中1个注射自身红细胞(红细胞斑块),建立斑块内出血模型,另2个斑块则分别注入等量的生理盐水(生理盐水斑块)或不注射(空斑块)作为对照。用免疫组化方法检测红细胞斑块、生理盐水斑块和空斑块的NF-κBp65亚基、IκBα表达和巨噬细胞浸润情况。结果红细胞斑块比生理盐水和空斑块有着更强的NF-κBp65亚基表达、更弱的IκBα表达、更明显的巨噬细胞浸润(P均<0.01)。结论斑块内出血后红细胞可明显地提高斑块的炎症水平,NF-κB涉及的炎症机制在此过程中扮演重要角色。

Objective To evaluate erythrocyte-induced inflammation of atherosclerotic plaques after intra-plaque hemorrhage,and to investigate its mechanism involving nuclear factorkappaB（NF-κB）.Methods After abdominal aorta arteries were injured by balloon over-stretch,a novel model of atherosclerotic plaques was established in 28 New Zealand white rabbits.Three distinct abdominal aortic plaques similar in thickness were identified in each rabbit by intravascular ultrasound（IVUS） imaging.One plaque received autologous erythrocytes（RBC plaque） to establish the model of intra-plaque hemorrhage.The other two plaques received an equal volume of normal saline（NS plaque） or received no injection（blank plaque） as controls.Macrophage infiltration and expressions of NF-κBp65 and IκBα were detected by immunohistochemical staining.Results RBC plaques showed more significant macrophage infiltration,higher NF-κB p65 expression and lower IκBα expression than NS and blank plaques（all P0.01）.Conclusion Erythrocytes can induce inflammation of plaques after intra-plaque hemorrhage.The mechanism involving NF-κB plays an important role in the process.