内皮状态和免疫活性细胞在动脉粥样硬化发展中作为缺血性卒中的一个原因的作用

N. Chuiko
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摘要

的目标。目的探讨动脉粥样硬化背景下脑血管内皮状态及免疫活性细胞在缺血性脑卒中发生中的作用。材料和方法。我们研究了50例缺血性脑梗死死亡患者、50例无CVD(脑血管疾病)表现的严重脑动脉粥样硬化患者和50例死亡原因与CVD和动脉粥样硬化无关的死亡患者(对照组)的脑血管。血管组织制备采用苏木精-伊红和马松三色染色,并用CD31/PECAM-1(内皮细胞标志物)Ab-1、CD4 (CD4 Ab-8)、CD8 (SP 16)、CD20 (CD20 Ab-1)、CD68和CD68/巨噬细胞标志物Ab-4进行免疫组化研究。结果。缺血性卒中和严重动脉粥样硬化时,脑血管内皮发生结构改变,表现为破裂、脱屑和脱落,形成脱屑内皮细胞簇。说到内皮损伤,不能认为改变只发生在宏观层面,细胞层面的内皮损伤要足够充分。免疫活性细胞在动脉粥样硬化的发展中起关键作用;动脉管腔表面的粘附、内皮下大量的巨噬细胞和内膜深处更成熟的巨噬细胞的存在表明这些细胞从血液流入动脉壁,积极促进动脉粥样硬化的形成。结论。内皮细胞形态改变导致的内皮内层紊乱有助于动脉粥样硬化斑块的形成。淋巴细胞和巨噬细胞构成了许多重要过程的分子基础,包括炎症反应和免疫反应
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Endothelium condition and role of immunocompetent cells in atherosclerosis development as a cause of ischemic stroke
The aim. To determine the state of the cerebral vascular endothelium and the role of immunocompetent cells in the ischemic stroke development on the background of atherosclerosis. Materials and methods. We studied cerebral vessels of 50 deaths with ischemic cerebral infarctions, 50 – with severe cerebral atherosclerosis without CVD (cerebrovascular disease) manifestation and 50 deaths, whose cause of death was not related to CVD and atherosclerosis (control group). Histological preparations of vessels were stained with hematoxylin-eosin and Masson Trichrome, and also immunohistochemical study was conducted using CD31/PECAM-1 (Endothelial Cell Marker) Ab-1, CD4 (CD4 Ab-8), CD8 (SP 16), CD20 (CD20 Ab-1) CD68 and (CD68/Macrophage Marker Ab-4) markers. Results. Under ischemic strokes and severe atherosclerosis the cerebral vessels endothelium acquires structural changes in form of rupture, desquamation and exfoliation, formation of desquamated endothelial cells clusters. Speaking of endothelial damage, it should not be supposed that changes should occur at the macroscopic level only, endothelial damage at the cellular level shall be sufficient enough. Immunocompetent cells are of key importance in atherosclerosis development; adhesion on the luminal surface of arteries, presence of a large number of these cells under the endothelium and of more mature macrophages in the intima depth indicates the influx of these cells, which actively potentiate atherosclerosis formation, from the blood into the artery wall. Conclusions . Disorders of the endothelial lining with changes in endothelial cells morphology contribute to the atherosclerotic plaque development. Lymphocytes and macrophages form the molecular basis of many important processes, including the inflammatory response and the immune response
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