Kristina Sonnenschein, Tibor Horváth, Maja Mueller, Andrea Markowski, Tina Siegmund, Christian Jacob, Helmut Drexler, Ulf Landmesser
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The present study was designed to evaluate the effects of moderate exercise training on in vivo endothelial repair capacity of early EPCs, and their nitric oxide and superoxide production as characterized by electron spin resonance spectroscopy analysis in subjects with metabolic syndrome.</p><p><strong>Methods and results: </strong>Twenty-four subjects with metabolic syndrome were randomized to an 8 weeks exercise training or a control group. Superoxide production and nitric oxide (NO) availability of early EPCs were characterized by using electron spin resonance (ESR) spectroscopy analysis. In vivo endothelial repair capacity of EPCs was examined by transplantation into nude mice with defined carotid endothelial injury. Endothelium-dependent, flow-mediated vasodilation was analysed using high-resolution ultrasound. Importantly, exercise training resulted in a substantially improved in vivo endothelial repair capacity of early EPCs (24.0 vs 12.7%; p < 0.05) and improved endothelium-dependent vasodilation. Nitric oxide production of EPCs was substantially increased after exercise training, but not in the control group. Moreover, exercise training reduced superoxide production of EPCs, which was not observed in the control group.</p><p><strong>Conclusions: </strong>The present study suggests for the first time that moderate exercise training increases nitric oxide production of early endothelial progenitor cells and reduces their superoxide production. 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引用次数: 42
摘要
背景:内皮功能障碍和损伤被认为是动脉粥样硬化发生和发展的重要因素。有研究表明,高强度运动训练可以增加早期内皮祖细胞(EPCs)的数量和血管生成特性。然而,运动训练是否刺激早期EPCs促进内皮损伤修复的能力及其潜在机制仍有待确定。本研究旨在评估适度运动训练对代谢综合征受试者早期内皮细胞体内内皮修复能力的影响,以及电子自旋共振光谱分析表征的内皮细胞一氧化氮和超氧化物的产生。方法与结果:24例代谢综合征患者随机分为8周运动训练组和对照组。利用电子自旋共振(ESR)光谱分析表征了早期EPCs的超氧化物生成和一氧化氮(NO)有效性。通过将内皮细胞移植到颈动脉内皮损伤的裸鼠体内,检测其在体内的内皮修复能力。利用高分辨率超声分析内皮依赖性、血流介导的血管舒张。重要的是,运动训练显著提高了早期EPCs的体内内皮修复能力(24.0% vs 12.7%;结论:本研究首次表明,适度运动训练可增加早期内皮祖细胞一氧化氮的产生,并减少其超氧化物的产生。重要的是,这与代谢综合征患者早期内皮细胞体内内皮修复能力的显著有益作用有关。
Exercise training improves in vivo endothelial repair capacity of early endothelial progenitor cells in subjects with metabolic syndrome.
Background: Endothelial dysfunction and injury are considered to contribute considerably to the development and progression of atherosclerosis. It has been suggested that intense exercise training can increase the number and angiogenic properties of early endothelial progenitor cells (EPCs). However, whether exercise training stimulates the capacity of early EPCs to promote repair of endothelial damage and potential underlying mechanisms remain to be determined. The present study was designed to evaluate the effects of moderate exercise training on in vivo endothelial repair capacity of early EPCs, and their nitric oxide and superoxide production as characterized by electron spin resonance spectroscopy analysis in subjects with metabolic syndrome.
Methods and results: Twenty-four subjects with metabolic syndrome were randomized to an 8 weeks exercise training or a control group. Superoxide production and nitric oxide (NO) availability of early EPCs were characterized by using electron spin resonance (ESR) spectroscopy analysis. In vivo endothelial repair capacity of EPCs was examined by transplantation into nude mice with defined carotid endothelial injury. Endothelium-dependent, flow-mediated vasodilation was analysed using high-resolution ultrasound. Importantly, exercise training resulted in a substantially improved in vivo endothelial repair capacity of early EPCs (24.0 vs 12.7%; p < 0.05) and improved endothelium-dependent vasodilation. Nitric oxide production of EPCs was substantially increased after exercise training, but not in the control group. Moreover, exercise training reduced superoxide production of EPCs, which was not observed in the control group.
Conclusions: The present study suggests for the first time that moderate exercise training increases nitric oxide production of early endothelial progenitor cells and reduces their superoxide production. Importantly, this is associated with a marked beneficial effect on the in vivo endothelial repair capacity of early EPCs in subjects with metabolic syndrome.