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背景:设想通过增加自体干细胞动员达到有效修复心脏缺血区的目的,因此找到可利用的特异而有效的干细胞动员剂成为关键所在。目的:观察心肌梗死时低氧诱导因子1α表达对骨髓间充质干细胞动员的影响。方法:将90只远交群SD大鼠结扎冠状动脉前降支建立急性心肌梗死模型,随机分为3组:低氧诱导因子1α反义寡核苷酸组给予低氧诱导因子1α反义寡核苷酸干预抑制大鼠梗死缺血组织的低氧诱导因子1α的表达,低氧诱导因子1α错义寡核苷酸组和对照组分别给予等量低氧诱导因子1α错义寡核苷酸和生理盐水。结果与结论:造模后30 h、7 d,对照组外周血骨髓间充质干细胞计数及血浆血管内皮生长因子水平与低氧诱导因子1α错义寡核苷酸组相近,但明显高于低氧诱导因子1α反义寡核苷酸组。造模后7 d,对照组心肌缺血组织低氧诱导因子1α蛋白、血管内皮生长因子蛋白及mRNA表达与低氧诱导因子1α错义寡核苷酸组相近,但明显高于低氧诱导因子1α反义寡核苷酸组。造模后7,14,28 d,对照组心肌缺血组织切片毛细血管密度分析与低氧诱导因子1α错义寡核苷酸组相近,明显高于低氧诱导因子1α反义寡核苷酸组。说明大鼠急性心肌梗死后高表达的低氧诱导因子1α与骨髓间充质干细胞动员、启动一系列心肌组织自我修复过程有因果关系。
BACKGROUND: Assuming the goal of effectively repairing the ischemic area of the heart by increasing mobilization of autologous stem cells, finding the specific and efficient stem cell mobilization available becomes the key. Objective: To observe the effect of hypoxia inducible factor 1α expression on the mobilization of bone marrow mesenchymal stem cells in patients with myocardial infarction. Methods: Acute myocardial infarction (AMI) model was established in 90 outdated SD rats with ligation of the anterior descending coronary artery and then randomly divided into 3 groups: HIF-1α antisense oligonucleotide group was given hypoxia-inducible factor-1α Nucleotide intervention inhibited the expression of hypoxia inducible factor 1α in rats with ischemic infarction. Hypoxia inducible factor 1α missense oligonucleotide group and control group were given the same amount of hypoxia inducible factor 1α missense oligonucleotide And saline. RESULTS AND CONCLUSION: The counts of bone marrow mesenchymal stem cells and the level of plasma vascular endothelial growth factor in control group were similar to those in hypoxia inducible factor 1α missense oligodeoxynucleotides at 30 h and 7 d after modeling, but were significantly higher than those in low Oxygen inducible factor 1 alpha antisense oligonucleotide group. At 7 days after model establishment, the expressions of hypoxia inducible factor 1α protein, vascular endothelial growth factor protein and mRNA in the control group were similar to those in the hypoxia inducible factor 1α missense oligonucleotide group, but significantly higher than those in hypoxia inducible factor 1α antisense oligonucleotide group. At 7, 14 and 28 days after modeling, capillary density analysis of myocardial ischemia in control group was similar to hypoxia inducible factor 1α missense oligonucleotide group, which was significantly higher than that in hypoxia inducible factor 1α antisense oligonucleotide group. It shows that there is a causal relationship between the high expression of HIF-1α and the mobilization of bone marrow mesenchymal stem cells and the initiation of a series of myocardial tissue self-repair process after acute myocardial infarction in rats.