Exercise Training Improves Functions of Endothelial Progenitor Cells in Patients with Metabolic Syndrome

Abstract Background Endothelial progenitor cells (EPCs) play an important role in maintaining endothelial function. Metabolic syndrome (MetS) is associated with EPC dysfunction. Although physical exercise has a beneficial impact on EPC activity, its mechanism is not completely clear yet. Objective The purpose of this study is to investigate the effects of physical exercise on the functions of EPCs and the underlying mechanisms in patients with MetS. Methods Volunteers with MetS were divided into exercise group (n=15) and control group (n=15). Before and after 8 weeks exercise training, EPCs were isolated from peripheral blood. Colony forming unit (CFU) assay, tube-formation assay, the protein expression of endothelial nitric oxide synthase (eNOS), phosphatidylinositol-3-kinase (PI3-K) and protein kinase B (AKT) were determined. A probability value <0.05 was considered to indicate statistical significance. Results After 8 weeks, the number of CFUs was significantly increased in the exercise group compared to the control group (p<0.05). In addition, we observed a significant decrease of homeostasis model assessment for insulin resistance (HOMA-IR), endothelin-1, high-sensitive C-reactive protein, and homocysteine levels in the exercise group. Exercise intervention could also enhance tube-formation capacity of EPCs and increase phosphorylation level of eNOS, PI3-K and AKT. Conclusion Physical exercise enhanced the functions of EPCs. The mechanism may be related to exercise, activating the PI3-K/AKT/eNOS pathway.

【背景】内皮祖细胞（Endothelial progenitor cells, EPCs）在维持血管内皮功能中发挥关键作用。代谢综合征（Metabolic syndrome, MetS）与内皮祖细胞功能障碍存在密切关联。尽管体力运动对内皮祖细胞活性具有积极调控作用，但其具体分子机制尚未完全明确。【研究目的】本研究旨在探讨体力运动对代谢综合征患者内皮祖细胞功能的影响及其潜在作用机制。【方法】将代谢综合征患者志愿者分为运动组（n=15）与对照组（n=15）。在8周运动训练周期前后，从受试者外周血中分离内皮祖细胞。通过集落形成单位（Colony forming unit, CFU）实验、管形成实验检测内皮祖细胞功能，并测定内皮型一氧化氮合酶（endothelial nitric oxide synthase, eNOS）、磷脂酰肌醇-3-激酶（phosphatidylinositol-3-kinase, PI3-K）及蛋白激酶B（protein kinase B, AKT）的蛋白表达水平。以P<0.05作为差异具有统计学意义的判定标准。【结果】8周干预后，运动组的集落形成单位数量较对照组显著升高（P<0.05）。此外，运动组患者的胰岛素抵抗稳态模型评估指数（homeostasis model assessment for insulin resistance, HOMA-IR）、内皮素-1、高敏C反应蛋白及同型半胱氨酸水平均显著降低。运动干预还可增强内皮祖细胞的管形成能力，并提升eNOS、PI3-K及AKT的磷酸化水平。【结论】体力运动可有效改善代谢综合征患者的内皮祖细胞功能，其潜在机制可能与激活PI3-K/AKT/eNOS信号通路相关。