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目的:探讨AGEs通过刺激SDF-1/CXCR4轴信号系统对心肌微血管内皮细胞的增值、迁移、管样结果形成的影响以及AMD3100对其的干预作用。方法:用不同浓度的AMD3100作用于浓度为200mg/L的AGEs共孵育的CMECs24h,用MTT法检测细胞活力及增殖能力,并选择合适的干扰浓度(抑制效果居中)。随机选取加入AGEs200ml/L的CMECs,加入合适浓度的AMD3100,分别作用24、48、72h,采用MTT法测定AGEs处理前后细胞增值率的变化,并检测AMD3100对增值率的影响;毛细血管管腔样结构形成实验检测对CMECs血管新生的影响和AMD3100对其阻断作用的影响。结果:心肌微血管内皮细胞增殖能力和迁移能力在24h、48h、72h有显著增强;并促进了心肌微血管内皮细胞管样形成(vsP<0.05);CXCR4受体阻断剂AMD3100作用于细胞后,可以显著阻断AGEs对心肌微血管内皮细胞增殖能力和迁移能力和管腔形成(vsP<0.05)的影响。结论:AGEs在早期显著增强了心肌微血管内皮细胞的增殖、迁移和管样结构形成的能力,其作用机制可能与SDF-1/CXCR4轴信号通路有关。
Objective: To investigate the effects of AGEs on the proliferation, migration and tube-like formation of cardiac microvascular endothelial cells by stimulating the SDF-1 / CXCR4 signaling system and the intervention effect of AMD3100. Methods: CMECs incubated with AGEs at a concentration of 200 mg / L for 24 h were treated with different concentrations of AMD3100 for 24 h. The viability and proliferation of CMECs were assayed by MTT assay and the appropriate interference concentration was selected. CMECs supplemented with 200 ml / L of AGEs were randomly selected and treated with appropriate concentrations of AMD3100 for 24, 48 and 72 hours respectively. The cell proliferation rate was measured by MTT assay before and after AGEs treatment. The effect of AMD3100 on proliferation rate was evaluated. Effect of Structure Formation Test on Angiogenesis in CMECs and the Effect of AMD3100 on Its Blockage. Results: The proliferation and migration of myocardial microvascular endothelial cells were significantly enhanced at 24h, 48h and 72h, and promoted the formation of tubular microvascular endothelial cells (vsP <0.05). After CX31 receptor antagonist AMD3100 was applied to cells, Significantly blocked the effects of AGEs on the proliferation, migration and lumen formation of myocardial microvascular endothelial cells (vsP <0.05). CONCLUSION: AGEs significantly enhances the proliferation, migration and tube-like structure formation of myocardial microvascular endothelial cells in early stage, which may be related to the SDF-1 / CXCR4 axis signaling pathway.