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肺泡形成基因P311在支气管肺发育不良中的作用 被引量:1

Function of Alveoli Formation Gene-P311 in Bronchial Pulmonary Hypoplasia
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摘要 目的:了解肺泡形成基因P311在支气管肺发育不良(BPD)中的作用;方法:64只早产昆明小鼠随机均分为空气组和高氧组,空气组置于室内,高氧组置于密闭的氧浓度>90%的氧舱中复制BPD动物模型;分别于造模后第1、3、7及14天取小鼠肺组织,分别采用苏木精-伊红染色观察小鼠肺组织病理改变鉴定造模是否成功,实时荧光定量聚合酶链式反应(Real-time PCR)法检测P311基因mRNA表达水平。结果:早产小鼠肺组织发育不成熟,高氧组随着吸氧时间的延长,小鼠表现反应迟钝、体重增长缓慢、毛发发涩无光泽、鼻尖发绀、呼吸急促,肉眼见肺组织表面有散在甚至弥漫的淤血点、小血管扩张充血,第3天镜下见肺泡腔内有炎性细胞浸润,第7天肺泡腔增大、肺间质增生,第14天肺泡腔内间质增生、少数肺泡融合、肺泡数量减少、肺泡结构简单化,说明BPD模型造模成功;第3天时2组P311基因mRNA表达量最高,随后下降;高氧组P311基因mRNA表达水平均高于同一时点空气组(P<0.05)。结论:长时间吸入高浓度氧成功构建支气管肺发育不良的动物模型,P311基因可能是影响肺损伤修复的调控因子。 Objective: To investigate the function of alveoli formation gene P311 in bronehopulmo- nary dysplasia (BPD). Method: A total of 64 premature mice were divided into air group and high oxygen group; air group was placed in the normal air, high oxygen group was placed in airtight oxygen chamber with oxygen concentration 90% to make BPD model. All subjects were taken the lung tissue 1,3,7 and 14 days after molding. HE staining was used to observe the lung tissue pathological changes and authenticate whether the model building was successful. The P311 gene expression level was detect by real - time quantitative polymerase chain reaction. Results: The lung tissue of premature mice did not develop mature; with the extension of time that the high oxygen group mice showed following reac- tions : slow reaction, slow growth in weight, lackluster hair, cyanotic nasal tip, short breath. The lung tissue surface had congestion points scattered, dilation and congestion of small blood vessels could be observed by naked eyes. 3 days after molding, the alveolar cavity was infiltrated with inflammatory cells, 7 days after molding, alveolar space increased and lung interstitial hyperplasia were found. Alveolar interstitial hyperplasia, some alveolar fusion and alveolar structure simplified 14 days after molding. These explained the model building was successful. The P311 gene levels in high oxygen group and air group increased on the 3rd day and then decreased. Compared with the air group, the P311 gene expression level was higher in high oxygen group ( P 〈 0.05 ). Conclusion: Inhaled high concentration oxygen for a long time can successfully build BPD model. P311 gene may be a regulatory factor of lung injury repair.
出处 《贵阳医学院学报》 CAS 2015年第7期688-691,共4页 Journal of Guiyang Medical College
基金 贵州省科技厅科研项目[黔科合J字(2011)2250号]
关键词 肺泡 支气管肺发育不良 肺泡形成基因 动物模型 基因表达 alveoli bronchopulmonary dysplasia alveoli formation gene animal model gene ex-pression
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参考文献14

  • 1陈超,袁琳.早产儿支气管肺发育不良的病因及危险因素[J].中国实用儿科杂志,2014,29(1):5-7. 被引量:55
  • 2Zhao LQ,Leung JK,Yamamoto H,et al.Identification of P311 as a potential gene regulating alveolar generation.American Journal of Respiratory[J].Cell Molecular Biology,2006(1):48-54.
  • 3早产儿支气管肺发育不良发生率及高危因素的多中心回顾调查分析[J].中华儿科杂志,2011,49(9):655-662. 被引量:194
  • 4Jiang D,Liang F,Fan J,et al.Regulation of lung injury and repair by Toll-like receptors and hyaluronan[J].Nat Med,2005(11):1173-1179.
  • 5Park HS,kim SR,Lee YC.Impact of oxidative stress on lung diseases[J].Respirology,2009(1):27-38.
  • 6Aslam MB,Aveja R,Liang OD,et al.Bone marrow stromal cells attenuate lung injury in a murine model of neonatal chronic lung disease[J].Am J Respir Crit Care Med,2009(11):1122-1130.
  • 7Van HT,Byrne R,Bonnet S,et al.Airway delivery of mesenchymal stem cells prevents arrested alveolar growth in neonatal lung injury in rats[J].Am J Respir Crit Care Med,2009(11):1131-1142.
  • 8Jiunn SJ,Yaw DL,Hsiu CC,et al.Activation of the Renin-Angiotensin System in Hyperoxia Induced Lung Fibrosis in Neonatal Rats[J].Neonatology,2011(101):47-54.
  • 9Paliwal S,Shi J,Dhru U,et al.P3l1 binds to the latency associated protein and downregulates the expression of TGF-β1and TGF-β2[J].Biochem Biophys Res Commun,2004(4):1104-1109.
  • 10Thurlbeck M.Pathology of the lung[M].New York:Thieme Medical,1995:37-87.

二级参考文献44

  • 1董永绥.婴儿巨细胞病毒性肝炎(上)[J].临床儿科杂志,2006,24(1):74-77. 被引量:69
  • 2Hentschel J, Berger TM, Tschopp A, et al. Population-based study of bronchopulmonary dysplasia in very low birth weight infants in Switzerland. Eur J Pediatr, 2005, 164:292-297.
  • 3Korhonen P, Tammela O, Koivisto AM, et al. Frequency and risk factors in bronchopulmonary dysplasia in a cohort of very low birth weight infants. Early Hum Dev, 1999, 54:245-258.
  • 4Sullivan JL. Iron, plasma antioxidants and the 'oxygen radical disease of prematurity'. Am J Dis Child, 1988, 142 : 1341-1344.
  • 5Williamson P, Griffiths G, Norfolk D, et al. Blood transfusions and human recombinant erythropoietin in premature newborn infants. Arch Dis Child, 1996, 75 :F65-68.
  • 6Demirel N, Bas AY, Zenciroglu A. Bronchopulmonary Dysplasia in Very Low Birth Weight Infants. Indian J Pediatr, 2009, 76: 695-698.
  • 7Jonsson B, Li YH, Noaek G, et al. Downregulatory cytokines in tracheobronchial aspirate fluid from infants with chronic lung disease of prematurity. Acta Paediatr, 2000, 89 : 1375-1380.
  • 8Sche|onka RL, Katz B, Waites KB, et al. Critical appraisal of the role of Ureaplasma in the development of bronchopulmonary dysplasia with metaanalytic techniques. Pediatr Infect Dis J, 2005, 24 : 1033-1039.
  • 9Speer CP. Inflammation and bronchopulmonary dysplasia. Se-min Neonatol, 2003, 8:29-38.
  • 10Tapia JL, Agost D, Alegria A, et al. Bronchopulmonary dysplasia, very low birth weight, risk factors, resource utilization, neonates. J Pediatr, 2006, 82:15-20.

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