2型糖尿病患者外周血内皮祖细胞数量变化及机制探讨
摘要
目的:探讨2型糖尿病(T2DM)患者内皮祖细胞(EPCs)的数量变化,为进一步防治T2DM患者的血管系统并发症提供依据。方法:110例患者,将其分为无糖尿病组及糖尿病组,并将糖尿病组按糖化血红蛋白水平再次分组。对入选者取清晨空腹静脉血测定EPCs数量、糖化血红蛋白(HbA1c)、人基质细胞衍生因子1α(SDF-1α)、活性氧(ROS)、内皮型一氧化氮合酶(eNOS),对其进行比较。结果:糖尿病组与无糖尿病组相比,EPCs数量、SDF-1α水平下降,ROS水平升高,差异有统计学意义(P<0.05);eNOS总量在两组之间差异无统计学意义(P>0.05)。在糖尿病组内,HbA1c>7%组与≤7%组间EPCs数量下降,ROS水平升高,差异有统计学意义(P<0.05)。结论:T2DM患者外周血EPCs数量减少,高血糖环境引起内皮细胞ROS大量生成是EPCs数量减少的可能机制之一。
引文
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[2]Liew A,McDermott J H,Barry F,et al.Endothelial progenitor cellsfor the treatment of diabetic vasculopathy:panacea or Pandora’sbox[J].Diabetes Obes Metab,2008,10(5):353
[3]Avogaro A,de Kreutzenberg S V,Fadini G.Endothelial dysfunc-tion:causes and consequences in patients with diabetes mellitus[J].Diabetes Res Clin Pract,2008,82(Suppl 2):S94
[4]Isabelle P,David J,Shahin R.The SD-1/CXCR4 ignaling pathway:a molecular hub modulating neoangiogesis[J].Trends Immunol,2007,28(7):299
[5]Churdchomjan W,Kheolamai P,Manochantr S,et al.Comparisonof endothelial progenitor cell function in type 2 diabetes with goodand poor glycemic control[J].BMC Endocrine Disorders,2010,10:5
[6]Fadini G P,Miorin M,Facco M,et al.Circulating endothelial pro-genitor cells are reduced in peripheral vascular complications oftype 2 diabetes mellitus[J].J Am Coll Cardiol,2005,45(9):1449
[7]Du X L,Edelstein D,Dimmeler S,et al.Hyperglycemia inhibitsendothelial nitric oxide synthase activity by posttranslational mod-ification at the Akt site[J].J Clin Invest,2001,108(9):1341
[8]Ho F M,Lin W W,Chen B C,et al.High glucose-induced apopto-sis in human vascular endothelial cells is mediated through NF-kappaB and c-Jun NH2-terminal kinase pathway and preventedby PI3K/Akt/eNOS pathway[J].Cell Signal,2006,18(3):391
[9]Kc S,Carcamo J M,Golde D W.Vitamin C enters mitochondria viafacilitative glucose transporter 1(Glut1)and confers mitochondri-al protection against oxidative injury[J].FASEB J,2005,19(12):1657
[10]Callaghan M J,Ceradini D J,Gurtner G C.Hyperglycemia-inducedreactive oxygen species and impaired endothelial progenitor cellfunction[J].Antioxid Redox Signal,2005,7(11-12):1476
[11]Tamarat R,Silvestre J S,Le Ricousse-Roussanne S,et al.Impair-ment in ischemia-induced neovascularization in diabetes:bonemarrow mononuclear cell dysfunction and therapeutic potential ofplacenta growth factor treatment[J].Am J Pathol,2004,164(2):457
[12]Gallagher K A,Liu Z J,Xiao M,et al.Diabetic impairments in NO-mediated endothelial progenitor cell mobilization and homing arereversed by hyperoxia and SDF-1 alpha[J].J Clin Invest,2007,117(5):1249