DPI抑制血管紧张素Ⅱ介导的内皮细胞凋亡和NOX4表达

目的观察DPI对血管紧张素Ⅱ（AngⅡ）介导的内皮细胞凋亡和NOX4表达的影响。方法倒置显微镜下观察人脐静脉内皮细胞形态；实验设对照组、AngⅡ组（10^-7mol／L AngⅡ处理16h）和DPI干预纽（10^-7mol／L AngⅡ加10μmol／L DPI处理16h）；用RT-PCR检测NOX4 mRNA水平；Hoechest染色观察细胞凋亡。结果AngⅡ组细胞凋亡与对照组相比明显增多，而DPI干预组细胞无明显改变；AngⅡ组hUVECs中NOX4 mRNA表达上调与对照组相比差异有显著性；而DPI干预组hUVECs中NOX4 mRNA表达与对照组相比差异无显著性，DPI干预组hUVECs中NOX4 mRNA表达与AngⅡ组相比差异有显著性。结论DPI抑制AngⅡ介导的内皮细胞凋亡和NOX mRNA表达。

DPI Inhibiting Apoptosis and NADPH Oxidase 4 Expression of hUVECs Induced by AngⅡ

Objective To observe the influence of DPI on apoptosis and NOX4 mRNA expression in hUVECs stimulated by Ang Ⅱ . Methods Morphology of hUVECs was observed by inverted microscope, hUVECs were divided into three groups： control group （ treated without Ang Ⅱ for 16 hours）, Ang Ⅱ （ treated with 10^-7 mol/L Ang Ⅱ for 16 hours） and DPI intervention group（treated with 10^-7 mol/L Ang Ⅱ plus 10μmol/l DPI for 16 hours）, mRNA expression of NOX4 was detected by RT-PCR. Cell apoptosis was observed by Hoechest staining. Results The results showed that apoptosis of hUVECs in Ang Ⅱ group was more than that in DPI intervention group, mRNA expression of NOX4 was increased in hUVECs treated with Ang Ⅱ （P〈0.05, vs control group）. After treated with DPI, mRNA expression of NOX4 in hUVECs decreased （P〉0.05, vs control group, P〈0.05, vs Ang Ⅱ group）. Conclusion DPI inhibits apoptosis and NADPH oxidase 4 expression of hUVECs induced by AngⅡ.