目的:应用应变率探讨不同左心室构型的原发性高血压患者左心室长轴方向应变－应变率成像的变化,及其与EF、FS及二尖瓣血流测量评价左室功能的对照研究。方法:采用M型、二维、多普勒超声及应变率成像技术,测量左室室壁厚度、左室内径、EF、FS,二尖瓣血流频谱E、A及左室平均应变ε,应变率S、e、a。结果:高血压离心性肥厚组EF、FS明显低于对照组,高血压其余各组EF、FS与对照组无统计学差异;收缩期应变率S应变ε在五组间差异均有显著性意义:高血压各组较正常对照组减小(I--Ⅴ呈递减);舒张期应变率e减低、a增高,e/a比值减小,各组间存在统计学差异(Plt;0.05); E/A,e/a结果大体一致。结论:应变率成像为临床提供了一个敏感、简便、可靠的评价原发性高血压患者左室心肌功能的指标。
ObjectiveTo investigate effects of high expression of miR-499a-5p on lung injury in rats with acute respiratory distress syndrome (ARDS) by targeting matrix metallopeptidase-16 (MMP-16).MethodsThe experiment set up sham operation group, model group, miR-499a-5p mimic group, MMP-16 group, miR-499a-5p mimic+MMP-16 group, D-ribofuranosylbenzimidazole (DRB, Nrf2 signaling pathway inhibitor) group, miR-499a-5p mimic+DRB group. A rat model of ARDS was constructed by cecal puncture. One hour before surgery, the transfection complex (50 μL) was injected into the trachea with a micro-syringe. DRB (5 mg/kg) was intraperitoneally injected 30 min before surgery. The expression levels of miR-499a-5p and MMP-16 in lung tissue were detected by RT-qPCR; Alveolar type Ⅱ epithelial cells of model group rats were separated and MMP-16 3 'UTR WT and MUT luciferase report plasmid were transfected into alveolar type Ⅱ epithelial cells with miR-499 respectively to verify the targeting relationship between miR-499 and MMP-16; the targeted relationship was verified by the dual luciferase reporter gene; lung injury was observed by hematoxylin-eosin staining; The level of inflammatory factors in bronchoalveolar lavage fluid (BALF) and the level of oxidative stress in lung tissue were detected by enzyme-linked immunosorbent assay; The expression levels of NAD(P)H: quinone oxidoreductase 1 (NQO1), heme oxygenase (HO)-1, and nuclear factor-erythroid 2-related factor 2 (Nrf2) proteins in lung tissues were analyzed by Western blotting.ResultsmiR-499a-5p was down-regulated in the lungs of ARDS model rats (P<0.01), while MMP-16 was highly expressed (P<0.01); miR-499a-5p and MMP-16 3'UTR regions had binding sites, and miR-499a-5p directly targeted negative regulation of MMP-16 expression (P<0.01); overexpression of miR-499a-5p significantly reduced the right lung wet-to-dry weight ratio in the ARDS rats (P<0.05), reduced lung tissue damage (P<0.01), and reduced tumor necrosis factor α, interleukin (IL)-1β and IL-6 levels in BALF (P<0.01), decreased malondialdehyde and myeloperoxidase levels in lung tissue, increased total anti-oxidant capacity (P<0.01), and up-regulated NQO1, HO-1, Nrf2 protein expression in lung tissue (P<0.01). However, this phenomenon was significantly reversed after the addition of MMP-16 and DRB.ConclusionOverexpression of miR-499a-5p attenuates lung injury in rats with ARDS by targeting negative regulation of MMP-16 via activating the Nrf2 signaling pathway.