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作 者:赵诣林[1] 马李杰[1] 陈向军[1] 常蕊静[1] 梁丽峰[1] 李佩佩[1] 金发光[1]
机构地区:[1]第四军医大学唐都医院呼吸内科,陕西西安710038
出 处:《中华肺部疾病杂志(电子版)》2013年第1期17-19,28,共4页Chinese Journal of Lung Diseases(Electronic Edition)
基 金:军队"十一五"攻关项目(08G-102);陕西省攻关项目(2008K14-08)
摘 要:目的探讨核转录因子-5(NFAT5)在海水淹溺性肺水肿中表达的变化及作用。方法40只180~200 g SD大鼠随机分为五组:对照组(NG),海水灌注1 h,2 h,3 h,4 h组,每组8只大鼠。灌注组经气管插管灌注4 ml/kg海水。不同时间点将大鼠处死,并将肺组织取出。计算肺湿干比(W/D)、伊文思蓝法检测肺通透指数(LPI)、逆转录-聚合酶链(RT-PCR)检测肺组织中NFAT-5及相关渗透压基因表达变化,同时进行病理形态学检查。结果肺组织病理形态学显示,海水灌注组肺组织出血,水肿,肺泡间隔明显增厚;灌注1 h组的W/D值较对照组W/D值显著增高(P<0.01);灌注组肺通透指数显著高于对照组(P<0.01),W/D值,LPI随时间的增加而逐渐减轻。RT-PCR结果表明,海水淹溺后NFAT5及渗透压保护相关基因的mRNA表达迅速增高,4 h后达到最高峰。结论在海水淹溺发生后,NFAT5表达显著增高,可进一步刺激有机渗透物质的增加,通过在高渗条件下维持细胞内外渗透压的平衡,减轻肺水肿,可能是治疗肺水肿的有效新途径。Objective To explore the mechanism and expression of nuclear factor of activated T cells 5 ( NFAT5 ) in the acute lung injury model induced by seawater drowning in rats. Methods 40 Sprague-Dawley (SD) rats, which were weighing 180-200 g each (5-7 weeks) , were randomly divided into 5 groups: a normal control group ( n = 8 ), 1 h, 2 h, 3 h and 4 h seawater group ( n = 8 ). Before being administered seawater (4 ml/kg body weight) through the trachea, 3% pentobarbital sodium (2.0 g/kg) intraperitoneal injection were given to the rats in order to anesthetised. The expression of NFAT5 were detected by qRT-PCR. The degree of pulmonary edema were evaluated by wet to dry ratio and LPI. Pulmonary histological changes were investigated by HE. Results Seawater aspiration induced injuries of the lung alveolar structures, such as edema, focal hemorrhage, distortion, thickened alveolar wall and the infiltration of inflammatory cells. In contrast, normal lung tissue architecture were existed in the normal group. The W/D ratio and LPI were significantly increased after seawater aspiration when compared with normal control. The noteworthy change oceured at 1 h after seawater aspiration and then gradually decreased, P 〈 0.01. The expression of NFAT5 mRNA was remarkably higher in seawater group than in normal group. Conclusion NFAT5 plays a key role in PE-SWD by regulates the transcription of transporters such as BGT1, AR and Taut to accumulate the osmolytes in order to maintain cellular homeostasis.
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