肺泡形成基因p311在高氧肺损伤中作用的分析-analysis of the role of pulmonary alveolar forming gene p311 in hyperoxia-induced lung injury.docxVIP

第二部分肺泡形成基因P311在高氧所致肺损伤小鼠肺组织中的作用研究【摘要】目的：了解肺泡形成基因P311在高氧暴露所致肺损伤小鼠肺组织中可能的作用；方法：将64只（60日龄）成年昆明（KM）小鼠随机分为空气组和高氧组，空气组置于室内常压空气中饲养，高氧组暴露于同一室内密闭的氧舱中，持续吸入氧浓度90%的医用氧气，空气组及氧气组分别喂养第1天、3天、7天、14天后取其肺组织（每组8只），苏木精－伊红染色（Hematoxylin-eosinstaining）观察肺组织病理变化并鉴定造模是否成功；免疫组织化学染色和实时定量聚合酶链反应法（Real-TimePCR）检测P311表达和基因；酶联免疫吸附测定法(ELISA)检测P311蛋白；结果：成年小鼠高氧组随着吸入高浓度氧气时间的延长，可见炎性细胞浸润、肺泡充血、水肿、肺泡腔增大、肺间质增生等病理变化；免疫组织化学染色后P311主要分布在肺泡壁及肺泡隔膜生长点的肺组织中，在空气组小鼠肺组织中呈弱阳性反应，而在高氧组小鼠肺组织中呈强阳性反应；成年小鼠高氧组P311基因及蛋白表达较空气组增高（P0.05）；结论：随着吸入高浓度氧气时间的延长小鼠肺损伤逐渐加重，证明成功复制高氧肺损伤的动物模型。P311基因表达及蛋白含量在高氧组中均高于空气组,说明P311可能是高氧肺损伤后促进肺损伤修复的新的调控因子。【关键词】高氧；肺损伤；P311；IIITheStudyoftheRoleofAlveoliFormationGene-P311inHyeroxiaLungInjuryMajor:pediatricsPostgraduate:ZENGBaomeiSupervisor:WANGYuchuanPartOneTheExpressionandSignificanceofAlveoliFormingGene-P311inLungTissueofMiceaboutHighOxygenCausingbronchopulmonarydysplasia【Abstract】Objective:TostudytheexpressionandsignificanceofalveoliformationgeneP311inlungtissueofmicabouthighoxygencausingbronchopulmonarydysplasia.Methods:64newborn(4daysage)ofKMmiceweredividedintoairgroup(thecontrolgroup)andhighoxygengroup(theexperimentalgroup),eachgroupof32,respectivelybythemotherfeeding,everyfemalemousewith8~10newbornmice,airgroupinthenormalpressurefeeding,highoxygengroupsinthesameroomcontinuousinhaledoxygenconcentrationinairtightoxygenchamber90%ofthemedicaloxygen,airgroupandhighoxygengrouptakingthelungtissueafterrespectively1,3,7and14days(8ineachgroup),thenobservthelungtissuepathologicalchangesandauthenticatewhetherthemodelbuildingsuccessfulbyhematoxylin-eosinstaining;Furtherimmune-histochemicalstainingandreal-timequantitativepolymerasechainreactionmethodstodetectP311changeandthedistributionofgeneexpression;Byenzymelinkedimmune-sorbentassaymethodtodetectP311protein.Results:Thelungtissuepathologyshowsthathighoxygengroupcomparedwithaircontrolgroup,astheoxygeninhalinghighconcentrationswiththeextensionoftime,thelungtissueexpressasalveolarnumberdecrease,volumeincrease,pulmonarystructuresimplificationandmicrovasculardys