阻塞性睡眠呼吸暂停患者外周血内皮祖细胞及促血管生成因子水平研究
发布时间：2019-01-15 23:31
【摘要】：目的观察阻塞性睡眠呼吸暂停(OSA)患者外周血内皮祖细胞(EPC)不同亚族和促血管生成因子水平的变化,探讨不同程度OSA患者外周血EPC对血管修复的可能性。方法选取90例OSA患者和30例健康志愿者(对照组),根据睡眠呼吸暂停低通气指数(AHI)将90例OSA患者均分为轻、中、重度OSA组。密度梯度离心法提取单个核细胞,依据乙醛脱氢酶(ALDH)活性对EPC进行分选,流式细胞仪联合CD133、CD34、含激酶域插入片段受体(PE-KDR)相应细胞表面标志物测定CD133~~+KDR~+EPC及CD133~+CD34~+EPC、CD34~+KDR~+EPC、ALDHloCD34~+KDR~+EPC的水平。酶联免疫吸附试验(ELISA)测定患者外周血低氧诱导因子-1α(HIF-1α),血管内皮生长因子(VEGF)及基质细胞衍生因子-1α(SDF-1α)的水平。结果对于外周血CD133~+KDR~+EPC、CD133~+CD34~+EPC、CD34~+KDR~+EPC水平,重度OSA组中度OSA组轻度OSA组对照组(均P0.05);轻、中度OSA组的外周血ALDHloCD34~+KDR~+EPC水平高于对照组,重度OSA组低于其他3组(均P0.05);血清HIF-1α、VEGF均是重度OSA组中度OSA组轻度OSA组对照组,SDF-1α水平为重度OSA组中度OSA组轻度OSA组对照组(均P0.05)。结论 OSA患者可能都会诱导动员并招募大量无效EPC,其数量庞大,但直接参与修复内皮的ALDHloCD34~+KDR~+EPC并未增加,尤其对于重度OSA患者甚至有可能减少,OSA减弱了修复内皮的可能性,加重了内皮损伤,从而增加心血管事件的发生风险。
[Abstract]:Objective to observe the changes of (EPC) subpopulations and angiogenic factors in peripheral blood endothelial progenitor cells (EPC) in patients with obstructive sleep apnea (OSA) and to explore the possibility of blood vessel repair by peripheral blood EPC in patients with OSA. Methods 90 patients with OSA and 30 healthy volunteers (control group) were divided into mild moderate and severe OSA groups according to sleep apnea hypopnea index (AHI). Mononuclear cells were extracted by density gradient centrifugation. EPC was sorted according to the activity of acetaldehyde dehydrogenase (ALDH). Flow cytometry combined with CD133,CD34, was performed. The levels of CD133~~ KDR~ EPC and CD133~ CD34~ EPC,CD34~ KDR~ EPC,ALDHloCD34~ KDR~ EPC were measured by the corresponding cell surface markers of kinase domain insert fragment receptor (PE-KDR). The levels of hypoxia-inducible factor-1 伪 (HIF-1 伪), vascular endothelial growth factor (VEGF) and stromal cell derived factor-1 伪 (SDF-1 伪) in peripheral blood were measured by (ELISA). Results for peripheral blood CD133~ KDR~ EPC,CD133~ CD34~ EPC,CD34~ KDR~ EPC level, severe OSA group, moderate OSA group, mild OSA group, control group (P0.05); The level of peripheral blood ALDHloCD34~ KDR~ EPC in mild and moderate OSA group was higher than that in control group, and that in severe OSA group was lower than that in other three groups (P0.05). The serum levels of HIF-1 伪 and VEGF in severe OSA group, moderate OSA group, mild OSA group, and SDF-1 伪 level were significantly higher than those in severe OSA group, moderate OSA group, mild OSA group and control group (P0.05). Conclusion all patients with OSA may induce mobilization and recruitment of a large number of ineffective EPC, but the number of ALDHloCD34~ KDR~ EPC directly involved in endothelial repair does not increase, especially in patients with severe OSA. OSA weakens the possibility of endothelial repair. Increased endothelial damage increases the risk of cardiovascular events.
【作者单位】： 天津医科大学总医院呼吸科;天津医科大学代谢病医院内分泌研究所;
【基金】：国家自然科学基金资助项目(81270144,30800507,81570084,2015BAI12B00,2012BAI05B02)
【分类号】：R766
[Abstract]:Objective to observe the changes of (EPC) subpopulations and angiogenic factors in peripheral blood endothelial progenitor cells (EPC) in patients with obstructive sleep apnea (OSA) and to explore the possibility of blood vessel repair by peripheral blood EPC in patients with OSA. Methods 90 patients with OSA and 30 healthy volunteers (control group) were divided into mild moderate and severe OSA groups according to sleep apnea hypopnea index (AHI). Mononuclear cells were extracted by density gradient centrifugation. EPC was sorted according to the activity of acetaldehyde dehydrogenase (ALDH). Flow cytometry combined with CD133,CD34, was performed. The levels of CD133~~ KDR~ EPC and CD133~ CD34~ EPC,CD34~ KDR~ EPC,ALDHloCD34~ KDR~ EPC were measured by the corresponding cell surface markers of kinase domain insert fragment receptor (PE-KDR). The levels of hypoxia-inducible factor-1 伪 (HIF-1 伪), vascular endothelial growth factor (VEGF) and stromal cell derived factor-1 伪 (SDF-1 伪) in peripheral blood were measured by (ELISA). Results for peripheral blood CD133~ KDR~ EPC,CD133~ CD34~ EPC,CD34~ KDR~ EPC level, severe OSA group, moderate OSA group, mild OSA group, control group (P0.05); The level of peripheral blood ALDHloCD34~ KDR~ EPC in mild and moderate OSA group was higher than that in control group, and that in severe OSA group was lower than that in other three groups (P0.05). The serum levels of HIF-1 伪 and VEGF in severe OSA group, moderate OSA group, mild OSA group, and SDF-1 伪 level were significantly higher than those in severe OSA group, moderate OSA group, mild OSA group and control group (P0.05). Conclusion all patients with OSA may induce mobilization and recruitment of a large number of ineffective EPC, but the number of ALDHloCD34~ KDR~ EPC directly involved in endothelial repair does not increase, especially in patients with severe OSA. OSA weakens the possibility of endothelial repair. Increased endothelial damage increases the risk of cardiovascular events.
【作者单位】： 天津医科大学总医院呼吸科;天津医科大学代谢病医院内分泌研究所;
【基金】：国家自然科学基金资助项目(81270144,30800507,81570084,2015BAI12B00,2012BAI05B02)
【分类号】：R766
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