Mitchinson M J, Hothersall D C, Brooks P N, De Burbure C Y
J Pathol. 1985 Feb;145(2):177-83. doi: 10.1002/path.1711450205.
It has been suggested that macrophages in atherosclerotic plaques oxidize the lipid they contain, leading to necrosis in the plaque. Over 200 human aortic and coronary atherosclerotic plaques from 102 human necropsy subjects aged between 5 and 88 were, therefore, examined histologically for the presence of insoluble lipid (ceroid), thought to be a product of lipid oxidation. Ceroid was present in all the plaques but not in areas of diffuse intimal thickening. In early lesions the insoluble lipid was within membrane-bound vesicles in macrophage-like cells, many showing characteristic ring structures suggesting that membrane-associated oxidative systems might be responsible for rendering the lipid insoluble. Staining was increased by an oxidizing agent and abolished by a reducing agent. It is suggested that this distribution supports the concept of lipid oxidation by macrophages within the plaque.
有人提出,动脉粥样硬化斑块中的巨噬细胞会氧化其所含的脂质,导致斑块坏死。因此,对102名年龄在5岁至88岁之间的人类尸检对象的200多个主动脉和冠状动脉粥样硬化斑块进行了组织学检查,以寻找被认为是脂质氧化产物的不溶性脂质(脂褐素)。脂褐素存在于所有斑块中,但在弥漫性内膜增厚区域不存在。在早期病变中,不溶性脂质存在于巨噬细胞样细胞内的膜结合囊泡中,许多囊泡呈现出特征性的环状结构,这表明膜相关的氧化系统可能是使脂质不溶性的原因。氧化剂可增强染色,还原剂可消除染色。有人认为,这种分布支持了斑块内巨噬细胞氧化脂质的概念。