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目的观察地尔硫对人大血管内皮细胞缺氧损伤时线粒体膜电位的影响。方法将培养的血管内皮细胞分为对照组、单纯缺氧组和加入地尔硫卓后再缺氧组,应用激光共聚焦显微镜扫描,并测定标记的血管内皮细胞每秒钟线粒体膜电位值,观察缺氧前后人大动脉血管内皮细胞线粒体膜电位变化。结果与对照组相比,单纯缺氧组的线粒体膜电位水平显著降低(P<0.01);加入地尔硫后再进行缺氧组与单纯缺氧组相比,内皮细胞线粒体膜电位水平有显著升高(P<0.01),与对照组相比内皮细胞线粒体膜电位水平变化不明显(P>0.05)。结论缺氧引起血管内皮细胞线粒体膜电位降低;地尔硫艹卓可抑制缺氧损伤所致的线粒体膜电位的降低,从而具有稳定线粒体膜电位、保护血管内皮细胞的作用。
Objective To observe the effect of diltiazem on mitochondrial membrane potential of human vascular endothelial cells during hypoxia injury. Methods The cultured vascular endothelial cells were divided into control group, hypoxia group and hypoxia group after adding diltiazem. Laser scanning confocal microscopy was used to detect the mitochondrial membrane potential value of labeled vascular endothelial cells per second. The changes of mitochondrial membrane potential in human aortic vascular endothelial cells before and after. Results Compared with the control group, the level of mitochondrial membrane potential in hypoxia group was significantly decreased (P <0.01). Compared with hypoxia group, the level of mitochondrial membrane potential (P <0.01). Compared with the control group, the level of mitochondrial membrane potential in endothelial cells did not change significantly (P> 0.05). CONCLUSION: Hypoxia can reduce the mitochondrial membrane potential of vascular endothelial cells. Diltiazem can inhibit the decrease of mitochondrial membrane potential induced by hypoxia, thus stabilizing mitochondrial membrane potential and protecting vascular endothelial cells.