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目的观察盐酸地尔硫卓(合贝爽)对缺氧加血管紧张素Ⅱ致血管内皮细胞线粒体膜电位变化的保护作用。方法将培养的血管内皮细胞分为对照组、血管紧张素Ⅱ加缺氧组以及应用合贝爽后的血管紧张素Ⅱ加缺氧组,应用激光共聚焦显微镜扫描并测定标记的血管内皮细丙每秒钟线粒体膜电位值,观察不同因素作用后人体大动脉血管内皮细胞线粒体膜电位变化。结果①与对照组相比,血管紧张素Ⅱ加缺氧组的线粒体膜电位水平(17±6)显著降低(P<0.01);②与血管紧张素Ⅱ加缺氧组相比,加入合贝爽后再进行缺氧和血管紧张素Ⅱ作用组内皮细胞线粒体膜电位水平(28±8)有显著升高(P<0.01),与对照组(37±9)比较差异无统计学意义(P>0.05)。结论缺氧联合血管紧张素Ⅱ可引起血管内皮细胞线粒体膜电位降低;合贝爽可明显减轻缺氧联合血管紧张素Ⅱ所致的线粒体膜电位的降低。
Objective To observe the protective effect of diltiazem hydrochloride (HBS) on mitochondrial membrane potential changes induced by hypoxia and angiotensin Ⅱ in vascular endothelial cells. Methods The cultured vascular endothelial cells were divided into the control group, angiotensin Ⅱ plus hypoxia group, and the combined use of angiotensin Ⅱ plus hypoxia group, laser scanning confocal microscopy and determination of labeled vascular endothelial cells Mitochondrial membrane potential value per second, to observe the changes of mitochondrial membrane potential of human aortic endothelial cells after different factors. Results ① Compared with the control group, the level of mitochondrial membrane potential (17 ± 6) in angiotensin Ⅱ plus hypoxia group was significantly decreased (P <0.01); ② Compared with angiotensin Ⅱ plus hypoxia group, The level of mitochondrial membrane potential in endothelial cells (28 ± 8) was significantly increased after hypoxia and angiotensin Ⅱ treatment (P <0.01), but no significant difference compared with that of control group (37 ± 9) (P > 0.05). Conclusions Hypoxia combined with angiotensin Ⅱ can induce the decrease of mitochondrial membrane potential in vascular endothelial cells. Hiabanyang can obviously reduce the decrease of mitochondrial membrane potential induced by hypoxia and angiotensin Ⅱ.