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NOX4和eNOS在小鼠慢性缺氧肺血管重塑中的表达及意义 被引量:2

Expressions of NOX4 and eNOS in pulmonary vasculature in mouse model of chronic hypoxia
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摘要 目的观察内皮型一氧化氮合酶(eNOS)和NOX4在小鼠慢性缺氧肺动脉高压形成过程中的改变。方法用HE染色法和免疫组织化学法观察C57BL/6 J小鼠在常氧和慢性持续缺氧(10±0.5%O2)1、3、7、14 d后肺血管的改变及非肌型小血管α-SMA和eNOS蛋白表达的改变。用Real Time PCR法检测各组小鼠肺组织中eNOS和NOX4 mRNA的含量。结果 C57BL/6 J小鼠慢性缺氧后肺小动脉血管管壁增厚、肺泡内肺动脉α-SMA表达增加,肺组织eNOS和NOX4 mRNA以及肺动脉内皮细胞eNOS蛋白的表达随缺氧时间延长进行性升高。结论 eNOS和NOX4可能在慢性缺氧肺动脉高压的发病机制中发挥重要作用。 Objective To investigate the pulmonary vascular endothelial nitric oxide synthase (eNOS)and NOX4 expressions in mice following chronic hypoxia. Methods C57BL/6J male mice were exposed to either normoxia or hypoxia ( 10±0. 5% 02 ) for 1, 3, 7 days or 2 weeks. HE staining was performed to observe pulmonary vascular remodeling of chronic hypoxia in mice. lmmunohistochemisty applied for detecting eNOS and α-SMA protein. The real-time PCR was used to investigate eNOS and NOX4 mRNA . Results Mice exposed to hypoxia exhibited significant pulmonary vascular remodeling characterized by thickening of the vascular wall and muscularization of previously nonmuscularized more distal small vessels. The expressions of mRNA of eNOS or NOX4 were significantly increased in the lungs in chronically hypoxic mice compared with normoxia controls, The immunohistochemical staining using an isoform-specific eNOS antibody demonstrated significant increase in eNOS expression in the lung vascular endothelium. Conclusion Both NOX4 and eNOS may play important roles in the pathogenesis of chronic hypoxia pulmonary hypertension.
出处 《临床肺科杂志》 2011年第5期679-681,共3页 Journal of Clinical Pulmonary Medicine
关键词 缺氧 肺动脉高压 内皮型一氧化氮合酶 NOX4 NADPH氧化酶 hypoxia pulmonary hypertension endothelial nitric oxide synthase NOX4 NADPH oxidase
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