期刊文献+

血小板源性生长因子对新生大鼠高氧肺损伤的影响 被引量:6

Effect of Platelet-Derived Growth Factor on Lung Injury in Hyperoxia-Exposed Ne wborn Rats
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摘要 目的 探讨血小板源性生长因子 (PDGF)在新生大鼠高氧肺损伤中时空作用机制。方法 应用免疫组织化学法定位PDGF表达 ,反转录 聚合酶链反应 (RT PCR)检测各时间点 (生后 4、7、10、14d)PDGFmRNA水平。结果 随日龄增加 ,PDGF A、 B含量发生不同的变化。高氧暴露下PDGF BmRNA含量及其表达均显著高于空气组 (P <0 .0 5 ,<0 .0 1)。而PDGF AmRNA水平及其表达却显著低于空气组 (P <0 .0 5 ,P <0 .0 1)。结论 高氧降低PDGF A水平 ,增加PDGF B含量。PDGF A、 B共同参与高氧暴露下肺组织损伤过程 ,是肺发育阻滞的重要因素。 Objective To investigate temporal and spatial effective mechanism of platelet-derived grow th factor(PDGF) to lung injury in newborn rats with hyperoxia-exposed. Methods Immunohistochemical methods were used to locate expression of PDGF,levels of PDG F mRNA were measured by reverse transcription polymerase chain reaction(RT-PCR) at age 4,7,10,14days. Results With the increasing ages,levels of PDGF-A and PDGF-B changed differently.Compa red with air group,levels of PDGF-B and PDGF-B mRNA increased significantly(P <0.05,P<0.01),but PDGF-A and PDGF-A mRNA reduced markedly (P<0.05,P <0.01)in hyperoxia-exposed group.Conclusions Levels of PDGF-A reduce and that of PDGF-B increase under hyperoxia exposure,P DGF-A、-B are involved in lung injury process and the importment factors in th e inhibition of lung development. J Appl Clin Pediatr,2005,20(2):113-115
出处 《实用儿科临床杂志》 CAS CSCD 北大核心 2005年第2期113-115,共3页 Journal of Applied Clinical Pediatrics
基金 湖北省科技厅重点资助项目 (2 0 0 0 2P160 1)
关键词 血小板源性生长因子 高氧 肺损伤 platelet derived growth factor hyperoxia lung injury
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参考文献16

  • 1钱莉玲,常立文,容志惠,张谦慎.维甲酸治疗新生大鼠高氧肺发育受抑对肺组织基质金属蛋白酶及其组织抑制剂表达的影响[J].实用儿科临床杂志,2002,17(6):602-604. 被引量:12
  • 2常立文.早产儿慢性肺部疾病的防治进展[J].实用儿科临床杂志,2004,19(2):81-83. 被引量:28
  • 3陈红兵,常立文.血小板源性生长因子致肺发育和肺损伤机制研究的新进展[J].实用儿科临床杂志,2004,19(4):313-315. 被引量:1
  • 4Churg A,Gilks B,Dai J.Induction of fibrogenic mediators by fine and ultrafinetitanium dioxide in rat tracheal explants[J].Am J Physiol,1999,277:975-982.
  • 5Warner BB,Stuart LA,Papes RA,et al. Functional and pathologica leffects of prolonged hyperoxia in neonatal mice[J].Am J Physiol,1998,275:110-117.
  • 6Buch S, Han RNN, Cabacungan J,et al.Changes in expression of platelet-derived growth factor and its receptors in the lungs of newborn rats exposed to air or 60% O2[J].Pediatr Res,2000,48(4):423-433.
  • 7Marumo T,Schini-Kerth VB,Fisslthaler B,et al.Platelet-derived growth factor-stimulated superoxide anion production modulates activation of transcription Factor NF-κB and expression of monocyte chemoattractant protein in human aortic smooth muscle cells[J].Circulation,1997,96:2361-2367.
  • 8Gurujeyalakshmi G, Hollinger MA, Giri SN. Pirfenidone inhibits PDGF isoforms in bleomycin hamster model of lung fibrosis at the translationl level[J].Am J Physiol,1999,276:311-318.
  • 9Rojas-Valencia L,Montiel F,Montano M,et al.Expression of a 2.8-kb PDGF-B/c-sis transcript and synthesis of PDGF-like protein by human lung fibroblasts[J].Chest,1995,108:240-245.
  • 10Simon AR, Takahashi S, Severgnini M,et al. Role of the JAK-STAT pathway in PDGF stimulated proliferation of human airway smooth muscle cells[J].Am J Physiol Lung Cell Mol Physi,2002,282:1296-1304.

二级参考文献18

  • 1[1]Saugstad OD. Brochopulmonary dysplasia and oxidative stress: are we closer to an understanding of the pathogenesis of BPD[J] ? Acta Pae diatr, 1997;86(12): 1277~ 1282
  • 2[2]Malpel S, Mendelsohn C, Cardoso WV. Regulation of retinoic acid sig naling during lung morphogenesis[J]. Development, 2000; 127 ( 14 ): 3057 ~ 3067
  • 3[3]Pierce RA, Shipley MJ. Retinoid-enhanced alveolization: identifying relevant downstream targets[J ]. Am J Respir Cell Mol Biol, 2000; 23 (2) :137~141
  • 4[4]Chailley-Heu B, Chelly N, Lelievre-Pegorier M, et al . Mild vitanin A deficiency delays fetal lung maturation in the rat[J]. Am J RespirCell Mol Biol, 1999;21(1) :89~96
  • 5[5]Massaro D, Massaro GD. Pulmonary alveous formation: critical pe riod,retinoid regulation and plasticity [ J ]. Novartis Found Symp, 2001 ;234:229~236;236~241
  • 6[6]Veness-Meehan KA, Bottone FG Jr, Stiles AD. Effects of retinoic acid on airspace development and lung collagen in hyperoxia-exposed new bom rats[ J ]. Pediatr Res, 2000; 48 (4): 434~ 444
  • 7[7]Nabeyrat E, Corroyer S, Besnard V, et al . Retinoic acid protects a gainst hyperoxia-mediated cell-cycle arrest of lung alveolar epithelialcells by preserving late Gl cyclin activities[J ]. Am J Respir Cell Mol Boil,2001 ;25(4) :507~514
  • 8[8]Pardo A, Barrios R, Maldonado V, et al . Gelatinases A and B are upregulated in rat lungs by subacute hyperoxia pathogenetic implications[J]. Am J Pathol, 1998; 153 (3) :833~ 844
  • 9[9]Radomski A, Sawicki G, Olson DM, et al . The role of nitric oxide and metalloproteinases in the pathogenesis of hyperoxia-induced lung injury in neonatal rats[J]. Br J Pharmcol, 1998; 125 (7): 1455 ~ 1462
  • 10[10]Frankenberger M, Hauck RW, Frankenberger B, et al . All transretinoic acid selectively down-regulates matrix metalloproteinase-9 (MMP-9) and up regulates tissue inhibitor of metalloproteinase-1 (TIMP-1) in human bronchoalveolar lavage cells [J]. Mol Med, 2001 ;7(4) :263~270

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