中文摘要：

stromal 的绑定导出房间的 factor-1 (SDF-1 ) 到半胱氨酸(C)-X-C 主题 chemokine 受体(CXCR4 ) 4 从骨头髓为茎和祖先房间 trafficking 作为一个关键信号出现了到发行量。我们的目的是在心肌的梗塞(MI ) 以后在愈合的过程期间调查 AMD3100 (一个特定的可逆 CXCR4 受体对手) 的每日的断断续续的管理的角色。Wistar 老鼠受到 MI， AMD3100 在外科以后 intraperitoneally 被注射。SDF-1 mRNA 表示被即时聚合酶链反应测量。组织学变化与 immunofluorescence 被分析，马森的三色的染色，并且小麦细菌凝集素。在外部血的白血球的数字被完全的血房间计数分析测量。矩阵 metalloproteinase-2/9 (MMP-2/9 ) 的活动被明胶 zymography 决定。在 infarcted 织物的 SDF-1 mRNA 的表示水平很快被提高(6 h ) ，在 24 h 达到顶点，然后在 7 天 post-MI 衰退了到正常水平。AMD3100 进一步在梗塞区域提高了 SDF-1 的增加。增加的白血球在对待 AMD3100 的组被观察。c-kit+ 干细胞和提高的 neovascularization 的动员被 AMD3100 扩充。另外， AMD3100 改进了室的改变，它被梗塞尺寸的减少揭示，可行 cardiomyocyte 代表性的区域和左室(LV ) LV 免费的墙厚度的扩大索引，和增加。MMP-2/9 的活动由 AMD3100 是起来调整的。在结论， AMD3100 的短期的断断续续的管理能在试验性的 MI 加速弯屈的愈合的过程并且是为 MI 的处理的潜在的治疗。

英文摘要：

The binding of the stromal cell-derived factor-lα （SDF-lα） to the cysteine （C）-X-C motif chemokine receptor 4 （CXCR4） has emerged as a key signal for stem and pro-genitor cells trafficking to the circulation from the bone marrow. Our aim was to investigate the role of daily inter-mittent administration of AMD3100 （a specific reversible CXCR4 receptor antagonist） during the healing process after myocardial infarction （MI）. Wistar rats were sub- jected to MI and AMD3100 was injected intraperitoneally after surgery. SDF-lα mRNA expression was measured by real-time polymerase chain reaction. Histology changes were analyzed with immunofluorescence, Masson＇s tri-chrome staining, and wheat germ agglutinin. The number of leukocytes in peripheral blood was measured by com-plete blood cell count analysis. The activities of matrix metalloproteinase-2/9 （MMP-2/9） were determined by gelatin zymography. The expression level of SDF-lα mRNA in the infarcted tissue was enhanced rapidly （6 h）, peaked at 24 h, and then declined to the normal level at 7 days post-MI. AMD3100 further enhanced the increase of SDF-lα in infarct area. Increased leukocytes were observed in AMD3100-treated groups. The mobilization of c-kit＋ stem/progenitor cells and enhanced neovasculari-zation were augmented by AMD3100. Additionally, AMD3100 improved ventricular remodeling, which was revealed by the decrease of infarct size, viable cardiomyo-cyte cross-sectional area and left ventricle （LV） expansion index, and the increase of LV free wall thickness. The activities of MMP-2/9 were up-regulated by AMD3100. In conclusion, short-term intermittent administration of AMD3100 could accelerate the wound healing process in experimental MI and be a potential therapy for the treat- ment of MI.