单核细胞趋化蛋白1和巨噬细胞炎性蛋白-1α在颅内动脉瘤壁内的表达

为探讨脑动脉瘤发生发展的病理过程 ,对 2例未破裂动脉瘤和 1 1例破裂的动脉瘤壁进行常规HE染色观察 ,并应用免疫组化方法观察单核细胞趋化蛋白 1 (MCP 1 )和巨噬细胞炎性蛋白 1α(MIP 1α)在颅内动脉瘤壁内的表达及位置。 2例正常脑动脉做对照比较。结果 :2例未破裂和 1 0例破裂动脉瘤HE染色 ,瘤壁由增厚的内膜和结缔组织外膜组成 ;纤维增厚的内膜有长梭形的成纤维细胞不规则排列 ;瘤壁全层有单核性细胞浸润。 1例破裂动脉瘤壁仅存玻璃样纤维结构 ,几乎不存在细胞成分 ;9例有附壁血栓 ,血栓呈机化表现。免疫组化 :正常动脉未见MCP 1和MIP 1α表达。 2例未破裂和 1 0例破裂动脉瘤壁内有MCP 1和MIP 1α的高表达 ,表达细胞多为成纤维细胞 ,颗粒沉积于胞质。阳性细胞呈局灶聚集 ,分布于动脉瘤内膜 ,多在排列紊乱的成纤维细胞、淋巴细胞聚集处。 1例破裂动脉瘤壁仅存玻璃样纤维结构 ,几乎不存在细胞 ,未见表达信号。动脉瘤附壁血栓内有MCP 1和MIP 1α的表达 ,表达细胞有成纤维细胞、微血管的内皮细胞 ,表达部位在胞质。未破裂的和破裂动脉瘤的病理表现和MCP 1、MIP 1α在动脉瘤壁内的局灶性的高表达 ,提示脑动脉瘤的发展是单核性细胞的不断聚集加强的慢性炎性过程

Monocyte Chemoattractant Protein-1 and Macrophage Inflammatory Protein-1αin Human Intracranial Normal Artery and Aneurysm Walls

Objective: To investigate the pathological course in the intracranial aneurysms. Methods: One case normal intracranial artery(from cortex fistulization), 11 cases ruptured aneurysms, two cases unruptured aneurysms were obtained from neurosurgical excision. Routine HE stain was used to observe histological characteristics, immunohistochemistry was used to observe the expression of monocyte chemoattractant protein-1(MCP-1)and macrocyte inflammation protein-1α(MIP-1α)in the walls of the normal artery and aneurysms(unruptured and ruptured). Result: By the HE strain the wall of the ruptured aneurysms(10 cases)and unruptured ones(2 cases)consisted of incrassated intima and connectivum extima. The fibroblast in the intima was arrayed in the disorder. Monocyte-like cells could be seen in the whole aneurysm wall. In one case of aneurysm wall(ruptured)glass-like fiber structure was left over, and few cells could be seen. Nine cases of mural thrombus could be found. The thrombus represented with organization. Immunohistochemistry: MCP-1 and MIP-1α were not detectable in the normal artery; the immunohistochemistry signal of MCP-1 and MIP-1α could be observed upregulated in the ruptured aneurysms(10 cases)and unruptured ones(2 cases), often in the intima. MCP-1 and MIP-1α appeared to be expressed by Fibroblast cell in its cytoplasm. Monocyte-like cells had little cytoplasm, the signal was seldom seen. The immunohistochemistry signal was discontinuous in the intima, MCP-1 and MIP-1α expressed where fibroblast and monocyte-like cells assembled. One case of ruptured aneurysms had no signal because there were no cells, only glass-like fiber. Mural thrombus had upregulated signal of MCP-1 and MIP-1α in the cytoplasm of fibroblasts and endotheliocytes of its micrangium. Conclusion: the pathological representation of the ruptured and unruptured aneurysms and the upregulated expression of MCP-1 and MIP-α in the aneurysm wall suggest that the development of the aneurysm may be a course of the chronic inflammation whose main inflammatory cells are monocyte-like cells.