| Abdominal aortic aneurysm ( AAA) represent a potentially fatal disorder that is characterized by segmental dilatation of the aortic wall and pathologic remodeling of the extracellular matrix. Although we can pay effective clinical treatment to the heavier AAA by aortic reconstruction and endovascular repair, the unclearing to the machanism of AAA directly influenced the prevention and cure effect. At present, it has been videly accepted that the inflammatoKy infiltration is correlated with the matrix metalloproteinases ( MMPs ) release. The active MMPs degrade elastic and collagen fiber, leading to the formation of AAA. The macrophages is the main source of infiltrating cells, while monocyte chemo-tactic protein-1 (MCP-1) has important regulation effect to the macrophages infiltration. So we observed the gene expression of MCP-1 in rats AAA model to explore their role in the early AAA.Methods48 wistar rats were divided into 4 experimental group and 4 control group by random and the animal model of AAA was constructed by perfusing elastase. Aortic diameter was measured before perfusion, after perfusion and before specimen collection, and the dilation rate was calculated. The specimen were obtained 3 day, 1 week, 2 week, 4 week after perfusion and were divided into 2 parts. The sections were snap frozen in liquid nitrogen for western blotting or maken section in freezing microtome. Elastin staining and CD68 ( macrophage specific antigen) immunohistochemical staining were used to detect the loss of e-lastin fiber and macrophages infilfration in aortic tissue in different period,whilein situ hybridization and Western blotting was applied to investigate the gene expression of MCP-1.ResultsIn experimental group, abdominal aorta dilated slightly (dilation rate 19. 5% ) in 3 day group; after that the dilation accelerated and developed the most marked aneurismal dilation at 2 week ( dilation rate 107. 0% ). In experimental group, the smooth muscle cells and endothelial cells lost their orders, with elastic lamina deformation rupture in 3 day ~ 1 week. There is obvious damage in 2 week; elastic fiber degraded and diminished; abundant inflammatory cells infiltrated into the aortic wall. Experimental group showed CD68 positive expression located media and adventitia which reached the peak at 2 week. In experimental group,MCP-1 mRNA expressed earlier and strongly expressed at 1 week, the protein expression of MCP-1 reached the peak at 2 week, which showed significant difference compared with other time phase (P < 0.01).ConclusionCompared with clinical research, animal model has obvious dominance in the study of pathogenesis of early AAA. Elastase induced aneurismal model is most vadely used in AAA study, which has similar pathology process with human AAA in many aspect such as inflammatory infiltration and endogenous MMPs production. Inflammatory cell infiltration closely correlated with the loss of elas-tin and collagen fiber during the whole processes of AAA. Macrophages are the important components of inflammatory cell, and it can release MMPs degradating extracellular matrix, we illustrated the basic pathologic process in the early AAA:when degeneration and damage of abdominal aorta occure by all kinds of factors, the expression products of MCP-1 induce macrophages adherence and aggregation in the injury aorta, which aggravate the lesion. In addition, the releasing of MMPs and other cytoactive material degrate the elastin and collagen fiber , dilate the aorta, result in the formation of AAA. Therefore, whether inhibi-ting the faction of infiltrating macrophages and related gene expression by medical or genetic therapy will be useful to AAA is to be studied in the near future.
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