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作 者:陈国兵[1] 许峰[2] 卢仲毅[2] 匡凤梧[2] 王兴勇[2]
机构地区:[1]福建医科大学附属厦门第一医院儿科,361003 [2]重庆医科大学附属儿童医院PICU,400014
出 处:《中国小儿急救医学》2008年第5期448-450,共3页Chinese Pediatric Emergency Medicine
摘 要:目的探讨地塞米松对新生大鼠高氧肺损伤时水通道蛋白1(AQP1)表达的影响及其对肺损伤的可能保护机制。方法新生Wistar大鼠32只随机分为空气组、高氧组、空气+地塞米松组、高氧+地塞米松组。第3天取肺组织,采用逆转录.聚合酶链反应(RT-PCR)和免疫组织化学法检测AQP1的mRNA表达和分布变化;并对肺湿/干重比(W/D)、支气管肺泡灌洗液(BALF)中的蛋白含量、肺通透指数及组织病理学改变进行对比分析。结果高氧暴露第3天肺组织出现出血、炎性细胞浸润和水肿,肺W/D、BALF蛋白含量、肺通透指数明显升高;地塞米松干预组肺损伤程度减轻,测定值降低。空气组、高氧组、高氧+地塞米松组AQP1mRNA相对吸光度比值分别为0.70±0.04、0.42±0.03、1.04±0.04,各组间差异有显著性(P〈0.05);与空气组相比,高氧组AQP1mRNA表达明显降低,高氧+地塞米松组AQP1mRNA表达显著上调;AQP1蛋白表达与其mRNA变化一致。结论高氧肺损伤时大鼠肺AQP1表达下调;地塞米松干预对肺损伤有保护作用,上调肺AQP1的表达可能是其作用机制之一。Objective To investigate the effect of dexamethasone on aquporin-1(AQP1) expression in the lung of hyperoxia-exposed newborn rats and to explore the protective mechanism of dexamethasone in lung injury. Methods Thirty-two newborn Wistar rats were randomly divided into 4 groups: room-air group, hy- peroxia-exposure group, room-air group treated with dexamethasone and hyperoxia-exposure group treated with dexamethasone. Lungs were harvested on the third day. The lung AQP1 mRNA expression and the protein location were detected by reverse transcription-polymerese chain reaction (RT-PCR) and immunohistochemistry. In addition, the wet-to-dry weight ratio(W/D), the protein content of broncho alveolar lavage fluid (BALF), lung permeation index and histological changes in lung were measured respectively. Results On the third day after hyperoxia-exposure, lung tissues appeared congestion, inflammatory cells exudation and edema. The lung W/D, the protein content in BALF and the lung permeation index in hyperoxia group were significandy higher than those in room-air group. In contrast, lung injury degree relieved in hyperoxia group treated with dexamethasone. The expressions of AQP1 mRNA in room-air group, hyperoxia group and hyperoxia group treated with dexamethasone were 0.70 ± 0.04, 0.42 ± 0.03 and 1.04 ± 0.04 respectively, and there was signiflcant difference (all P 〈 0.05 ). Compared with room-air group, the expressions of AQP1 mRNA was than that in hyperoxia group, while the expression was upregulated in hyperoxia group treated with dexamerce, The changes of AQP1 protein level was persistent with the changes of AQP1 mRNA expression. Conclusion The expressions of lung AQP1 downregulates in hyperoxia-indueed lung injury. Dexamethasone can upregulates the expressions of lung AQP1, which might he one of the protective mechanisms against hyperoxia -induced lung injury.
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