红细胞生成素对慢性肾衰竭大鼠外周血内皮祖细胞SDF-1及其受体表达的影响*

 目的：观察红细胞生成素（EPO）对慢性肾衰竭（CRF）大鼠外周血内皮祖细胞（EPCs）归巢因子表达的影响。方法：采用分阶段5/6肾切除制备大鼠CRF模型。实验动物随机分为3组：假手术组、CRF组和EPO治疗组。从第3周开始，治疗组大鼠每次皮下注射重组人EPO 50 U/kg，每周3次，共6周。8周时取其外周血分离与培养EPCs，并检测EPCs的功能。采用实时荧光定量PCR和Western blotting检测外周血EPCs基质细胞衍生因子1 （SDF-1）及其受体（CXCR4）、EPO及其受体（EPOR）mRNA和蛋白的表达。结果：与CRF组比较，EPO治疗可上调外周血EPCs中SDF-1和CXCR4 mRNA及蛋白的表达（均P<0.05）；此外，EPO还可上调CRF大鼠外周血EPCs的 EPO及EPOR mRNA和蛋白的表达（均P<0.05）。结论：EPO对慢性肾衰竭大鼠外周血EPCs的动员可能与其增加外周血EPCs的 SDF-1及其受体表达有关。

Effects of erythropoietin on expression of SDF-1 and its receptor in peripheral blood endothelial progenitor cells from rats with chronic renal failure

AIM:To investigate the effects of erythropoietin (EPO) on the expression of homing factors in peripheral blood endothelial progenitor cells (EPCs) from rats with chronic renal failure (CRF). METHODS:The CRF model was established by a two-stage 5/6 nephrectomy procedure in rats. Experimental rats were randomly divided into three groups: sham operation group, CRF model group and EPO treatment group. From the third week after the second stage of 5/6 nephrectomy procedure, rats in EPO treatment group received subcutaneous injection of human recombinant EPO at 50 U/kg every time and three times a week for 6 weeks, and then all the rats were sacrificed. EPCs were isolated from rat peripheral blood and primarily cultured. The mobilization, angiogenesis and functional activity of EPCs in vitro were detected. The mRNA and protein expression of EPO, EPO receptor (EPOR), stromal cell-derived factor 1 (SDF-1) and CXC chemokine receptor 4 (CXCR4) in EPCs was also detected by the methods of real-time PCR and Western blotting. RESULTS:Compared with CRF model group, the expression of EPO and EPOR in EPCs in EPO treatment group was significantly up-regulated (P<0.05). Moreover, the expression of SDF-1 and its receptor CXCR4 in EPCs was also up-regulated by administration of EPO (P<0.05). CONCLUSION: EPO can mobilize EPCs from CRF rat peripheral blood, which may be associated with the increased expression of SDF-1 and its receptor CXCR4.