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目的:研究骨髓干细胞向心肌梗死区迁移归巢的机制,探讨其对心肌梗死的作用。方法:制备大鼠心肌梗死模型,梗死心肌边缘区注射血管内皮生长因子(VEGF),病理学检测心肌梗死后心肌细胞分泌的细胞因子变化及其与CD34+骨髓间充质干细胞(BMCs)迁移归巢之间的关系。结果:心肌梗死后1 d VEGF表达最高(2 351±112)pg/m l,随时间的推移,7 d时降至(1 875±87)g/m l(P<0.01),其浓度迅速降低,至14 d时已降至(212±95)pg/m l,假手术组始终无VEGF的表达;在心肌梗死区边缘局部注射VEGF后24 h可见CD34+BMCs数为(24.4±5.2)个/HP,未注射VEGF的心肌梗死区也可见CD34+骨髓干细胞浸润,但CD34+BMCs数仅为(7.5±2.0)个/HP,P<0.01;心肌梗死后14 d,注射VEGF组与未注射组心肌梗死区毛细血管密度分别为(11.38±1.31)和(3.12±1.32),P<0.01。结论:在心肌梗死区边缘局部注射VEGF,可以促进CD34+BMCs向心肌梗死区归巢,可能参与毛细血管增生和坏死心肌的修复。
Objective: To study the mechanism of bone marrow stem cells migrating to homing in myocardial infarction area and to explore its effect on myocardial infarction. Methods: The model of myocardial infarction in rats was established. The vascular endothelial growth factor (VEGF) was injected into the marginal area of infarcted myocardium. The changes of cytokines secreted by cardiomyocytes after myocardial infarction were detected by pathology and their migration to CD34 + bone marrow mesenchymal stem cells (BMCs) The relationship between. Results: The expression of VEGF was the highest (2 351 ± 112) pg / ml at 1 d after myocardial infarction and decreased to (1875 ± 87) g / ml on the 7th day (P <0.01) (212 ± 95) pg / ml on day 14, and there was no VEGF expression in sham operation group. The number of CD34 + BMCs in 24 h after local injection of VEGF in the marginal area of myocardial infarction was (24.4 ± 5.2) / HP , The infiltration of CD34 + bone marrow stem cells was also observed in the infarcted area without VEGF injection, but the number of CD34 + BMCs was only (7.5 ± 2.0) /HP, P <0.01; on the 14th day after myocardial infarction, VEGF and non-injected myocardial infarction The area capillary density was (11.38 ± 1.31) and (3.12 ± 1.32), P <0.01. CONCLUSION: Local injection of VEGF at the margin of myocardial infarction area can promote the homing of CD34 + BMCs to myocardial infarction area, which may be involved in the repair of capillary hyperplasia and necrotic myocardium.