粒细胞集落刺激因子对大鼠实验性心肌梗死的治疗作用

目的：探讨粒细胞集落刺激因子（G0CSF）动员的自体骨髓来源的干细胞对大鼠急性心肌梗死动物模型的治疗作用。方法：用异丙肾上腺素（ISO）复制大鼠急性心肌梗死动物模型，用骨髓干细胞动员剂G－CSF动员自体骨髓干细胞释放和迁移至心肌梗死部位，于用ISO后24，48h和2周后杀死大鼠，取出心脏，用免疫组化和HE染色方法检测动物模型心梗区的CD34^ 单个核细胞浸润以及心肌细胞和血管的再生情况。结果：用ISO后24h,G-CSF处理组大鼠心梗区可见大量CD34^ 单个核细胞浸润，并用CD34^ 的新生心肌细胞生长，2周后瘢痕组织较少，毛细血管浸密度明显高于对照组，而用ISO后24h，对照组心梗坏死区有大量以中性粒细胞为主的炎症细胞浸润，无CD34^ 细胞浸润及新生心肌细胞生长，2周后出现较大量的瘢痕组织。结论：G－CSF能促进心肌梗死后心肌细胞和血管的再生，减小心肌梗死的范围，用G－CSF动员自体骨髓干细胞来修复坏死心肌组织的“干细胞自身移植”疗法，可用于急性心肌梗死的治疗。

Effects of G- CSF on myocardial infarction in experimental rats

Objective To investigate the effects G-CSF-mobilized bone marrow stem cells on myocardial infarction in experimental rats. Methods Three hours after injection of isoprenaline(ISO) interaperitoneally to develop acute ischemic model, rat bone marrow stem cells were mobilized by G-CSF and migrated to the site of myocardial infarction. Hearts were harvested from 24 hours to 2 weeks after administration of ISO for histopathological examination. Immunohistochemisty and HE stain were used to detect infiltration of CD34 + monocytes and the regeneration of myocytes and angiogenesis in the infarct zones. Results 24 hours after administration of ISO, large number of infiltrative monocytes and some regenerative myocytes with positive expression of CD34 + were found in the infarct zones of the G-CSF treatment group, while majority of the infiltrative inflammatory cells in control group were neutrophils and there were no infiltrative cells and myocytes with positive expression of CD34 +; 2 weeks after administration of ISO, there were less scar and higher capillary density in the G-CSF treatment group than those in control group. Conclusion Neovascularization and regeneration of myocytes are enhanced and the infarct size is reduced by treatment of G-CSF in rats model of myocardial infarct. Mobilization of autologous bone marrow stem cells by G-CSF for regeneration of myocardium may be used for treatment of acute myocardial infarction.