有氧运动改善动脉粥样硬化病变的抗炎症机制研究

Study on Anti-inflammatory Mechanism of Aerobic Exercise Improving Atherosclerosis

目的:以apo-E基因缺陷小鼠建立动脉粥样硬化模型,通过观察有氧运动对主动脉壁炎性因子水平以及CD68阳性巨噬细胞浸润的影响,对有氧运动改善动脉粥样硬化病变的抗炎症机制进行探讨。方法:apo-E基因缺陷小鼠随机分为安静对照组和运动组(游泳运动,90 min/次,6次/周,周末休息,共持续10周),每组10只。10周后取小鼠主动脉冰冻切片,免疫组化方法测定主动脉壁细胞粘附分子-1(VCAM-1)、单核细胞趋化蛋白-1(MCP-1)和单核/巨噬细胞表面分子CD68的表达水平。结果表明,与对照组相比,1)运动组主动脉管壁的脂质斑块面积明显减小。2)运动组小鼠主动脉壁的VCAM-1和MCP-1的表达极显著下降(P<0.01)。3)单核/巨噬细胞表面分子CD68在运动组小鼠主动脉壁的表达极显著下降(P<0.01)。结论:10周有氧运动可极显著下调apo-E基因缺陷小鼠主动脉壁炎性因子VCAM-1和MCP-1的表达,同时减轻单核/巨噬细胞在主动脉壁的附着和侵润。提示有氧运动可通过显著改善动脉粥样硬化病变局部的炎症状态发挥抗动脉粥样硬化作用。

Objectives ： Took apoE-deficient mice to establish atherosclerosis model, the purpose of this paper is to observe the effects of aerobic exercise on inflammatory＇ factors and CD68 level in aortic wall, and to explore the an- ti-inflammatory mechanism of aerobic exercise improving atherosclerosis. Methods： Twenty apoE-deficient mice were randomly divided into control group （CG, n = 10） and exercise group （EG, n = 10） , EG mice participated in swimming （90 minutes/day, 6 days/week, 10 weeks）. After 10 weeks, the aorta was collected and done freez- ing section. The expressions of VCAM - 1, MCP - 1 and CD68 on aorta were measured by immunohistochemistry. Results： 1 ） The lipid-core plagues area in aorta is lower in EG than in CG. 2） Compared with CG, the expres- sions of VCAM - 1 and MCP - 1 in aorta of EG were significantly decreased （P 〈0.01 ）. 3） The expression of CD68 in EG was significantly decreased （P 〈 0.01 ）. Conclusion： Ten weeks aerobic exercise reduced the ex- pressions of VCAM - 1 and MCP - 1, and reduced the attachment and invasion of monocytes/macrophages in aortic wall, which suggested aerobic exercise could improve atherosclerosis by anti-inflammatory.