论文部分内容阅读
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 understand the erythrocyte-induced plaque inflammation after plaque hemorrhage and to explore the mechanism involved in NF-κB. Methods Twenty-eight New Zealand white rabbits were selected and atherosclerosis models were established by balloon-dwelling abdominal aorta. Three plaques of similar thickness were selected on the abdominal aorta of each animal by intravascular ultrasound (IVUS), of which 1 injected erythrocytes (erythrocyte plaque), established plaque hemorrhage model and the other 2 plaques The same amount of normal saline (normal saline plaque) or no injection (empty plaque) were injected as a control respectively. Immunohistochemistry was used to detect NF-κBp65 subunit, IκBα expression and macrophage infiltration in erythrocyte plaque, normal saline plaque and plaque. Results The erythrocyte plaques had stronger expression of NF-κBp65 subunit, weaker IκBα expression and more obvious macrophage infiltration (P <0.01) than saline and plaque. Conclusion Erythrocytes can significantly increase the plaque inflammation level after hemorrhage in plaque. The inflammatory mechanism involved in NF-κB plays an important role in this process.