[Objective] To observe the influence of granulocyte-colony stimulating factor (G-CSF) and stem cell factor (SCF) on the murine heart function and structure as well as local ischemia-related inflammation after acute myocardial infarction. [Methods] Ninety GDI mice were randomly grouped and then G-CSF /SCF (n =50) or saline solution (n =40) were applied for 6 days continuously. On day 3, myocardial infarction was induced in the mice of both groups. Three weeks later, ultrasound was used to determine heart function and the histological techniques were used to assess the cellular structure and the extent of local inflammation. [Results] The intervention of cytokines enhanced the murine cardiac output after acute myocardial infarction without the reduction of infarction area, induced cardiac cellular hypertrophy as well as the infiltration of white blood cell in ischemic region. [Conclusion] The intervention of G-CSF/SCF can improve murine heart function after myocardial infarction, however, unrelated to the cardiomyocyte regeneration. The bone marrow mobilization may aggravate the inflammatory reaction in ischemic cardiac tissue.%目的 了解粒细胞集落刺激因子(G-CSF)和干细胞因子(SCF)对小鼠心肌梗死后的心脏结构、功能以及缺血区炎症反应的影响.方法 90只CD1小鼠随机分组后,分别连续给予6天的G-CSF/SCF(n=50)或生理盐水(n=40).在干预的第三天制作小鼠的心肌梗死模型.术后3周利用心脏超声检测心功能,应用组织学技术检测心肌细胞结构改变以及判断组织的炎症程度.结果 细胞因子干预可以增加心肌梗死后心输出量,但不缩小心肌梗死的面积;同时可以诱导缺血区心肌细胞肥大以及促进白细胞在缺血区域的浸润.结论 G-CSF/SCF干预可以改善心肌梗死后小鼠的心功能,但与心肌再生无明显相关.骨髓动员可以加重缺血局部心肌组织的炎症反应.
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