中文摘要：

目的脂蛋白（a）[Lp（a）]水平增高是冠状动脉和周围血管疾病的独立危险因素。本研究拟在下肢缺血小鼠模型中观察Lp（a）对内皮祖细胞（EPC）向缺血组织归巢的影响并初步探讨其机制。方法从小鼠骨髓中分离诱导培养EPC。EPC经磷酸缓冲盐溶液（PBS）或Lp（a）（20mg／L）处理12h后，分别移植入下肢缺血小鼠，以荧光显微镜检测EPC归巢到缺血组织和血管发生能力。同时，EPC经PBS或Lp（a）处理后，以荧光显微镜、Westernblot检测Lp（a）对EPC黏附能力及相关基因表达的影响。结果整体实验发现，植入对照的EPC（PBS-EPC）后，下肢缺血区显示有大量归巢的EPC及血管腔样结构。与此相反，植入Lp（a）处理的EPCILp（a）-EPC]后，下肢缺血区仅显示有极少量归巢的EPC及毛细血管腔样结构。体外实验显示，对照组EPC黏附性能强，P-选择素糖蛋白配体1（PSGL-1）、CXCR4蛋白表达丰富。与对照组相比，Lp（a）减弱EPC的黏附能力及下调PSGL-1和CXCR4蛋白表达。结论Lp（a）抑制EPC归巢到下肢缺血组织．其机制可能与下调EPC的PSGL一1、CXCR4表达及降低EPC黏附性能有关。

英文摘要：

Aim High lipoprotein （a） [ （ Lp （a） ] level had been identified as an independent risk factor for coronary and peripheral blood disease. In this study, we investigatd the effect of Lp （a） on endothelial progenitor cells （EPC） homing to the sites of hindlimb ischemia tissues and its potential mechanisms. Methods After treatment with PBS or Lp（a） for 12 h, EPC were transplanted into the hindlimb ischemia mouse model by a tail intravenous injection. The homing and vasculogenesis of EPC were determined. On the other hand, EPC adhesion ability and related gene expression were detected in vitro. Results Lp（a） inhibited homing of EPC to the sites of ischemic tissues and weakened fuction of EPC vasculogenesis. Further, Lp（a） impaired EPC adhesion ability and down-regulated expression of P-selectin glycoprotein ligand-1 （PSGL-1） as well as CXCR4 in EPC in vitro. Conclusion Lp （a） inhibited EPC homing to the sites of hindlimb ischemic tissues possibly by lowering adhesion ability of EPC and PSGL-1, CXCR4 expression in EPC.