Reduced arterial elasticity is a hallmark of ageing in healthy humans and appears to occur independently of coexisting disease processes. 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. A total of 56 healthy male volunteers were divided into young (n ¼ 26) and elderly (n ¼ 30) groups. Large and small artery elasticity indices were noninvasively assessed using pulse wave analysis. The number of circulating EPCs was measured by using flow cytometry. Cells demonstrating DiI-acLDL and FITC-ulex lectin double-positive fluorescence were identified as EPCs. C1 large artery elasticity and C2 small artery elasticity indices were significantly reduced in the elderly group compared with the young group (11.7371.45 vs 16.8871.69 ml/mm Hg  10, Po0.001; 8.4071.45 vs 10.5871.18 ml/mm Hg  100, Po0.001, respectively). In parallel, the number of circulating EPCs was significantly reduced in the elderly group compared with the young group (0.1370.02 vs 0.1770.04%, Po0.05). The number of circulating EPCs correlated with C1 large and C2 small artery elasticity indices (r ¼ 0.47, Po0.01; r ¼ 0.4, Po0.01). The present findings suggest that the fall in circulating EPCs with subsequently impaired endothelial-cell repair and function contributes to reduced arterial elasticity in humans with ageing. The decrease in circulating EPCs may serve as a surrogate biologic measure of vascular function and human age.

Berberine (BR) has been proved to promote endothelial function. However, the exact mechanisms underlying the effect of BR on endothelial function are not completely clear. It has been demonstrated that endothelial progenitor cells (EPCs) contribute to improvement of endothelial function and C2 small artery elasticity index is a surrogate parameter for the clinical evaluation of endothelial function. We hypothesized that BR-induced mobilization of circulating EPCs is associated with BR-related improvement of endothelial function. To address this assumption, 15 healthy volunteers were recruited and received BR 0.4 g three times per day for 30 days. The number of circulating CD34/KDR double-positive cells as well as C1 large and C2 small artery elasticity indices were evaluated before and after BR therapy. The number of CD34/KDR doublepositive EPCs increased significantly after BR treatment (0.030 ± 0.020% vs 0.017 ± 0.010%, Po0.01). After 30-day BR therapy C2 increased significantly (6.21±2.80 ml per mm Hg  100 vs 4.06±2.67 ml per mm Hg  100, Po0.01) and C1 remained unchanged (10.79 ± 3.27 ml per mm Hg  10 vs 10.06 ± 2.08 ml per mm Hg  10, P40.05). The increment of CD34/KDR double-positive EPCs was positively correlated with the increment of C2 (r ¼ 0.68, Po0.01). We concluded that BR-induced mobilization of circulating EPCs contributes to improvement of small artery elasticity in healthy persons.

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