[Effects of macrophage infiltration and related gene expression on the pathogenesis of early abdominal aortic aneurysm]

To detect the pathogenic mechanism of early abdominal aortic aneurysm (AAA).

Pig elastinase was perfused into the abdominal aortae of 40 Wistar rats to construct AAA animal models. The diameter of abdominal aorta was measured and then the abdominal aorta was harvested from 10 rats on the postoperative days 3, 7, 14, and 28 respectively. The thoracic aorta was used as control. HE staining, elastic staining, and CD68 (macrophage specific antigen) immunohistochemical staining were used to detect the distribution of elastic fiber and macrophage infiltration in aortic tissue. In situ hybridization was applied to investigate the mRNA expression of monocyte chemotactic protein-1 (MCP-1) and matrix metalloproteinase-2 (MMP-2).

Three days after the operation, the expansion of abdominal aorta began to be seen and peaked 2 weeks after operation. Disruption of elastic fiber began to be found in the wall of abdominal aorta since 3 approximately 7 days after operation, and reached the maximum 2 weeks postoperatively. CD68 positive cell was not found in the wall of normal thoracic aorta and began to be found in the wall of abdominal aorta 3 approximately 7 days after operation. The expression of CD68 protein peaked on the day 14 with a significant difference from that on day 3 (t = 5.13, P < 0.01). The number of CD58 positive cells was remarkably decreased 4 weeks after operation in comparison with that 2 weeks after operation (t = 4.27, P < 0.01). The mRNA expression rates of MCP-1 and MMP-2 in the wall of abdominal aorta were at their maximal values, (31.5 +/- 5.7)% and (35.2 +/- 7.8)%, on the postoperative days 7 and 14 respectively, significantly higher than those at other time points (all P < 0.01). The MCP-1 and MMP-2 positive cells began to decrease since the 4th postoperative week.

Macrophage infiltration is parallel to MMP-2 mRNA expression and elastic fiber disruption in aortic tissue. MCP-1 mRNA expression, as a promoting factor, induces the macrophage infiltration, thus contributing to the development and progression of AAA.