摘要
客观: 在间充质的干细胞(MSC ) 上调查 MCP-1 的效果 homing 到在一只老鼠的受伤心肌层心肌的梗塞(MI ) 模型。方法: 老鼠心肌的梗塞模型被永久左前面的下降分支结扎建立。从施主老鼠的间充质的干细胞在 IMDM 是有教养的并且用 BrdU 标记。老鼠被划分成二个组。单核白血球趋化性的蛋白质 1 (MCP-1 ) 表达式被测量由在 situ 杂交和免疫组织化学在假冒操作或在在 MCP-1 察觉的 1， 2， 4， 7， 14 和 28 天帖子操作的 infarcted 心组织。老鼠与 MCP-1 被注射， anti-MCP-1 抗体或盐在在干预的心肌的梗塞以后的 4 天组织。然后， 5 ×的一个总数 10 ~ 在 PBS 的 2.5 ml 的 6 个房间通过尾巴静脉被注射。在 infarcted 心的标记的 MSC 的数字被数 3 天柱子注射。心脏的功能和血容器密度被估计 28 天柱子注射。结果: 自生的 MCP-1 表示在第一天被增加，在 7 ^(th ) 达到顶点白天并且此后减少了帖子 MI 并且在假冒的操作的心仍然保持未改变。在主人心的 MSC 丰富在 non-MI 组比那更充满 MI 组( P = 0.000 )，在主人心的 MSC 丰富更充满 MCP-1 在 anti-MCP-1 抗体和盐的注射的组比那注射了组( P = 0.000 )。心脏的功能在 MCP-1 更被改进比 anti-MCP-1 抗体和盐的注射的组(P= 0.000 ) 注射了组。在 MCP-1 的 Neovascularization 注射了显著地与另外的组的相比增加的组(P = 0.000 ) 。结论：心肌的 MCP-1 表示仅仅在早阶段柱子 MI 被增加。MCP-1 可以提高 MSC homing 到受伤的心并且由支持 neovascularization 改进心脏的功能。
Objective：To investigate the effect of MCP-1 on mesenchymal stem cells（MSCs） homing to injured myocardium in a rat myocardial infarction（MI） model. Methods：Rat myocardial infarction model was established by permanent left anterior descending branch ligation. Mesenchymal stem cells from donor rats were cultured in IMDM and labeled with BrdU. The Rats were divided into two groups. Monocyte chemotactic protein I（MCP-1） expression were measured by in situ hybridization and immunohistochemistry in the sham operated or infarcted hearts at 1, 2, 4, 7, 14 and 28 days post operation in MCP-1 detection group. The rats were injected with MCP-1, anti-MCP-1 antibody or saline 4 days after myocardial infarction in intervention group. Then, a total of 5 × 10^6 cells in 2.5 ml of PBS were injected through the tail vein. The number of the labeled MSCs in the infarcted hearts was counted 3 days post injection. Cardiac function and blood vessel density were assessed 28 days post injection. Results：Self-generating MCP-1 expression was increased at the first day, peaked at the 7^th day and decreased thereafter post MI and remained unchanged in sham operated hearts. The MSCs enrichment in the host hearts were more abundant in the MI groups than that in the non-MI group（P= 0.000）, the MSCs enrichment in the host hearts were more abundant in the MCP-1 injected group than that in the anti-MCP-1 antibody and saline injected groups （P = 0.000）. Cardiac function was improved more in MCP-1 injected group than anti-MCP-1 antibody and saline injected groups（P= 0.000）. Neovascularization in MCP-1 injected group significantly increased compared with that of other groups（P = 0.000）. Conclusion： Myocardial MCP-1 expression was increased only in the early phase post MI. MCP-1 may enhance MSCs homing to the injured heart and improve cardiac function by promoting neovascularization.
关键词
心肌梗塞
间叶干细胞
强心剂
单核细胞趋化蛋白-1
mesenchymal stem cells
homing
myocardial infarction
cardiac function
monocyte chemotactic protein 1
