年龄相关的循环内皮祖细胞变化与动脉弹性关系的研究

目的　研究年龄对循环内皮祖细胞及动脉弹性的影响,探讨循环内皮祖细胞水平与动脉弹性损伤的关系。方法　56例健康男性志愿者分成青年组(n=26)和老年组(n=30)。采用桡动脉脉搏分析法无创性评价健康志愿者大动脉弹性指数(C1 )和小动脉弹性指数(C2 ), 流式细胞仪测定外周血中CD34+单个核细胞的水平,单个核细胞体外培养2周,荧光显微镜鉴定FITC UEA I和DiI acLDL双染色阳性细胞为内皮祖细胞。结果　老年组与青年组相比较,C1 和C2 明显降低[C1(11. 73±1 .45)比(16 .89±1 .69)ml/mmHg×10, P<0. 001; C2 (8 .40±1 45)比(10. 58±1 .18)ml/mmHg×100, P<0 .001 ];循环内皮祖细胞数目明显减少[ ( 0 .13±0. 02 )比( 0 .17±0. 04 )%,P<0 .05];循环内皮祖细胞水平与动脉弹性指数变化呈正相关(r=0. 47, P<0. 01;r=0 .4, P<0. 01),荧光显微镜鉴定贴壁细胞FITC UEA I和DiI acLDL双染色阳性。结论　增龄导致循环内皮祖细胞数量减少,提示血管内皮修复能力下降和功能障碍,损伤动脉弹性,循环内皮祖细胞水平有可能作为评价血管功能的替代指标。

A study of association between age-related circulating endothelial progenitor cells and arterial elasticity

OBJECTIVE: Reduced arterial elasticity is a hallmark of aging in healthy humans independently of diseases and endothelial-cell injury and dysfunction may be responsible for this fall in arterial elasticity. We hypothesized that circulating endothelial progenitor cells (EPCs) are involved in endothelial repair and that lack of EPCs contributes to impaired arterial elasticity. METHODS: A total of 56 healthy male volunteers were divided into young (n = 26) and elderly (n = 30) groups. Large and small artery elasticity indices were non-invasively assessed by using pulse wave analysis. Flow cytometer was used to count the number of circulating CD34(+) mononuclear cells (MNCs), which were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. EPCs were characterized as adherent cells double positive staining for DiI-acLDL uptake and lectin binding with using flourescent microscope. RESULTS: C(1) (large artery elasticity index) and C(2) (small artery elasticity index) were significantly reduced in the elderly group compared with those in the young group (11.73 +/- 1.45 vs 16.89 +/- 1.69 ml/mm Hg x 10, P < 0.001; 8.40 +/- 1.45 vs 10.58 +/- 1.18 ml/mm Hg x 100, P < 0.001 respectively). In parallel, the number of circulating EPCs was significantly reduced in the elderly group compared with the young group (0.13 +/- 0.02 vs 0.17 +/- 0.04%, P < 0.05). The number of circulating EPCs correlated with C(1) large and C(2) small artery elasticity indices (r = 0.47, P < 0.01; r = 0.4, P < 0.01). Flourescent microscope was used to identify EPCs, which were double positive staining for DiI-acLDL uptake and lectin binding. CONCLUSION: The present findings suggested that the fall in circulating EPCs with subsequently impaired endothelial-cell repair and function might contribute to reduced arterial elasticity in humans with aging. The decrease in circulating EPCs could serve as a surrogate biologic measure of vascular function and human age.