【摘要】：目的觀察阻塞性睡眠呼吸暫停(OSA)患者外周血內(nèi)皮祖細(xì)胞(EPC)不同亞族和促血管生成因子水平的變化,探討不同程度OSA患者外周血EPC對(duì)血管修復(fù)的可能性。方法選取90例OSA患者和30例健康志愿者(對(duì)照組),根據(jù)睡眠呼吸暫停低通氣指數(shù)(AHI)將90例OSA患者均分為輕、中、重度OSA組。密度梯度離心法提取單個(gè)核細(xì)胞,依據(jù)乙醛脫氫酶(ALDH)活性對(duì)EPC進(jìn)行分選,流式細(xì)胞儀聯(lián)合CD133、CD34、含激酶域插入片段受體(PE-KDR)相應(yīng)細(xì)胞表面標(biāo)志物測(cè)定CD133~~+KDR~+EPC及CD133~+CD34~+EPC、CD34~+KDR~+EPC、ALDHloCD34~+KDR~+EPC的水平。酶聯(lián)免疫吸附試驗(yàn)(ELISA)測(cè)定患者外周血低氧誘導(dǎo)因子-1α(HIF-1α),血管內(nèi)皮生長(zhǎng)因子(VEGF)及基質(zhì)細(xì)胞衍生因子-1α(SDF-1α)的水平。結(jié)果對(duì)于外周血CD133~+KDR~+EPC、CD133~+CD34~+EPC、CD34~+KDR~+EPC水平,重度OSA組中度OSA組輕度OSA組對(duì)照組(均P0.05);輕、中度OSA組的外周血ALDHloCD34~+KDR~+EPC水平高于對(duì)照組,重度OSA組低于其他3組(均P0.05);血清HIF-1α、VEGF均是重度OSA組中度OSA組輕度OSA組對(duì)照組,SDF-1α水平為重度OSA組中度OSA組輕度OSA組對(duì)照組(均P0.05)。結(jié)論 OSA患者可能都會(huì)誘導(dǎo)動(dòng)員并招募大量無(wú)效EPC,其數(shù)量龐大,但直接參與修復(fù)內(nèi)皮的ALDHloCD34~+KDR~+EPC并未增加,尤其對(duì)于重度OSA患者甚至有可能減少,OSA減弱了修復(fù)內(nèi)皮的可能性,加重了內(nèi)皮損傷,從而增加心血管事件的發(fā)生風(fēng)險(xiǎn)。
[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 偽 (HIF-1 偽), vascular endothelial growth factor (VEGF) and stromal cell derived factor-1 偽 (SDF-1 偽) 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 偽 and VEGF in severe OSA group, moderate OSA group, mild OSA group, and SDF-1 偽 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.
【作者單位】： 天津醫(yī)科大學(xué)總醫(yī)院呼吸科;天津醫(yī)科大學(xué)代謝病醫(yī)院內(nèi)分泌研究所;
【基金】：國(guó)家自然科學(xué)基金資助項(xiàng)目(81270144,30800507,81570084,2015BAI12B00,2012BAI05B02)
【分類號(hào)】：R766

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