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单核细胞趋化蛋白-1、细胞间黏附分子-1和血管细胞黏附分子-1存在于实验大鼠早期动脉瘤扩张中。

MCP-1, ICAM-1 and VCAM-1 are present in early aneurysmal dilatation in experimental rats.

作者信息

Fan Jun, Li Xiang, Zhong Linlin, Di Jing, Liu Fang, Zhao Hai-Hua, Bai Shu-Ling

机构信息

Department of Tissue Engineering, Department of Human Anatomy, College of Basic Medicine, China Medical University, Shenyang, China.

出版信息

Folia Histochem Cytobiol. 2010 Sep 30;48(3):455-61. doi: 10.2478/v10042-010-0042-y.

Abstract

Recent studies have suggested that inflammation actively participates in ascending aortic aneurysm formation. The aim of the present study was to evaluate the expression changes of adhesion molecules and MMPs in an experimental model of ascending aortic aneurysm induced by ascending aorta banding in Wistar rats. Twelve rats developed aortic dilation after ascending aorta banding treatment, while nine normal animals underwent surgery without banding were used as controls. Light microscope and scanning electron microscope showed that the wall of the ascending aorta became disorganized as well as infiltration by inflammatory cells in aneurysmal rats. By using immunohistochemical techniques, a significant increase in the immunostaining of MCP-1 was observed in the aneurysmal wall as compared to the normal aortic wall. Under similar experimental conditions, we also found that the immunostaining of ICAM-1 and VCAM-1 was markedly increased in the aneurysmal wall. In addition, gelatin zymographic analysis showed that the expression and activities of MMP-2 and MMP-9 were remarkably enhanced in the ascending aorta of ascending aortic aneurysmal rats as compared to normal rats. These results demonstrate that MCP-1, ICAM-1 and VCAM-1 are involved in the pathogenesis of ascending aortic aneurysm and an increase in the immunostaining and activity of MMP-2 and MMP-9 may promote the progression of ascending aortic aneurysm.

摘要

近期研究表明,炎症在升主动脉瘤形成过程中发挥着积极作用。本研究旨在评估在Wistar大鼠升主动脉缩窄诱导的升主动脉瘤实验模型中黏附分子和基质金属蛋白酶(MMPs)的表达变化。12只大鼠在升主动脉缩窄处理后出现主动脉扩张,而9只未进行缩窄的正常手术动物作为对照。光学显微镜和扫描电子显微镜显示,升主动脉瘤大鼠的升主动脉壁结构紊乱,伴有炎性细胞浸润。通过免疫组化技术发现,与正常主动脉壁相比,动脉瘤壁中单核细胞趋化蛋白-1(MCP-1)的免疫染色显著增加。在相似的实验条件下,我们还发现动脉瘤壁中细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)的免疫染色明显增加。此外,明胶酶谱分析表明,与正常大鼠相比,升主动脉瘤大鼠升主动脉中MMP-2和MMP-9的表达及活性显著增强。这些结果表明,MCP-1、ICAM-1和VCAM-1参与了升主动脉瘤的发病机制,MMP-2和MMP-9免疫染色及活性的增加可能促进升主动脉瘤的进展。

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