期刊文献+

慢性阻塞性肺疾病大鼠支气管肺组织EGR-1、PDGF-BB的表达及普米克令舒干预的影响 被引量:1

Expression of EGR-1、PDGF-BB in chronic obstructive pulmonary disease model of rats and the interfention of pulmicort respules
下载PDF
导出
摘要 目的:探讨早期生长反应因子-1(EGR-1)、血小板源性生长因子-BB(PDGF-BB)在慢性阻塞性肺疾病(COPD)发病机制中的作用,并评价普米克令舒在COPD治疗中的效果。方法:用烟熏加气管内灌注内毒素的方法复制COPD大鼠模型,造模完成后给予雾化吸入普米克令舒两周,观察1周、2周、4周组,普米克干预组及各对照组大鼠的支气管肺组织病理变化,进行免疫组织化学染色和定量图像分析,以检测EGR-1、PDGF-BB蛋白质表达水平。结果:1各时间点模型组大鼠均有不同程度的COPD的病理改变,各对照组病理结构基本正常。普米克干预组与干预对照组相比病理表现无明显改善。2各时间点模型组大鼠肺间质结缔组织、支气管壁及小血管壁内可见棕黄色颗粒状或细丝状的EGR-1、PDGF-BB蛋白阳性染色。模型1周、2周、4周组大鼠的支气管肺组织中EGR-1、PDGF-BB的积分光密度(IOD)值与各对照组相比均有显著性差异。模型1周、2周、4周组大鼠的EGR-1、PDGF-BB的IOD值也有显著性差异。3雾化吸入普米克令舒后EGR-1、PDGF-BB表达与对照组相比均有明显下降。4EGR-1和PDGF-BB表达呈正相关。结论:1EGR-1、PDGF-BB可能参与COPD气道炎症进展。2EGR-1与PDGF-BB的表达水平呈正相关,二者的诱导表达机制尚需进一步研究。3COPD激素吸入两周可以降低EGR-1、PDGF-BB的表达水平,但并未引起明显病理改变。 Objective:To research the roles of early growth response-1(EGR-1)and platelet derived growth factor-BB (PDGF-BB)in the pathogenesis of inflammation of chronic obstructive pulmonary disease (COPD) ,and to evaluate the effect of Pulmicort Respules inhalation on COPD. Methods:The rat COPD models were established by passive cigarette smoking plus intratracheal instillation of lipopolysacchride(LPS),and after that the rats received inhalation of Pulmicort Respules for two weeks. The pathologic characteristics of airway and lung tissue were observed, and the expression of EGR-1 and PDGF-BB protein were measured by immunohistochemical stain in the rat model group lweek, 2week, 4week. Results: ① All model rats had pathologic changes of COPD in different degree, and the control groups had barely changes, and the pathological changes of rats of drug inhalation group were not dictinctly different from that of the inhalation control group. ②Strong positive stain of EGR-1 and PDGF-BB protein was found in the interstitial conncetive tissue ,the bronchial wall and the wall of blood vessels in the bronchial and lung tissue in the model groups. The integral optical density (IOD)of EGR-1 and PDGF-BB in model group 1week, 2week, 4week was significantly higher than that of control groups. There were significant differences in IOD of EGR-1 protein in model group lweek,2week,4week,and so did in IOD of PDGF-BB protein. ③ IOD of EGR-1 and PDGF-BB protein of drug inhalation group was significantly lower than that of inhalation control group. ④The expression of EGR-1 protein was positive correlated with that of PDGF-BB. Conclusion: ①EGR-1 and PDGF-BB may contribute to the process of inflammation of COPD. ②The expression of EGR-1 and PDGF-BB protein was positive correlated with each other, and how they influence each other need further research. ③ The inflammation in airway of rats inhaled Pulmicort Respules for two weeks was restrained to some extent, and significant pathologic changes were not ob
出处 《陕西医学杂志》 CAS 北大核心 2008年第5期525-528,542,共5页 Shaanxi Medical Journal
基金 泸州医学院资助课题(No05050)
关键词 肺疾病 慢性阻塞性/病理生理学 肺疾病 慢性阻塞性/药物疗法 肾上腺皮质激素/治疗应用 生长调节素类/代谢 生长物质/代谢 Pulmonary disease ,chronic obstructive/physiopathology Pulmonary disease ,chronic obstructive/drug therapy Adrenal cortex hormones/therapeutic use Somatomedins/metabolism Growth substances/metabolism
  • 相关文献

参考文献10

  • 1李红梅,崔德健,佟欣,庞宝森,高亚兵,王德文.熏香烟加气管注内毒素和单纯熏香烟法建立大鼠COPD模型[J].中国病理生理杂志,2002,18(7):808-812. 被引量:105
  • 2Liu LX,Tsai JC,William C. Aird Egr-1 gene is induced by the systemic administration of the vascular endothelial growth factor and the epidermal growth factor. Blood, 2000, 96(5) :1772-1781. 被引量:1
  • 3Paul R R, Manuel GC, John RH. Cigarette smoke- induced Egr-1 upregulates pro-inflammatory cytokines in pulmonary epithelial cells. Respir Cell Mol Biol, 2006, 35:314-319. 被引量:1
  • 4Jin Y, Nigel M,Thomas SE, et al. Lipopolysaccharide induction of the tumor necrosis, factor-a promoter in human monocytic cells, regulation by Egr-1, c-Jun and NF-kB transcription factors. Biological Chemistry, 1997, 272(28) : 17795-17801. 被引量:1
  • 5Yan SF, Lu JS, Xu LN, et al. Pulmonary expression of early growth response-1:biphasic time course and affect of oxygen concentration. Appl Physiol, 2000, 88 (6): 2303-2309. 被引量:1
  • 6Mausumee G,Mariaa-O'Connell A, Pawlinski R, et al. Lipopolysaccharide activation of the MEK-ERK1/2 pathway in human monocytic cells mediates tissue factor and tumor necrosis factor-α expression by inducing Elk-1 phosphorylation and Egr-1 expression. Blood, 2001, 98 (5):1429-1439. 被引量:1
  • 7刘建,彭东信,刘晓晴,朱朝霞,车东媛,赵时宇.肺炎支原体感染大鼠肺组织中PDGF-BB变化的免疫组织化学研究[J].中国组织化学与细胞化学杂志,2001,10(1):76-80. 被引量:8
  • 8Schwachtgen JL,Houston P,Campbell C, et al. Fluid shear stress activation of Egr-1 transcription in cultured human endothelial and epithelial cells is mediated via the extracellular signal-related kinase 1/2 mitogen-activated protein kinase pathway. Clin Invest,1998,101(11):2540- 2549. 被引量:1
  • 9Khachigian LM,Lindner V,Williams AJ,et al. Egr-1- induced endothelial gene expression: a common theme in vascular injury. Science, 1996 , 271 (5254):1427-1431. 被引量:1
  • 10Rupprecht HD, Sukhatme VP, Lacy J, et al. PDGF- induced Egr-1 expression in rat mesangial cells is mediated through upstream serum response elements. Renal Physiol, 1993,265 (3) : 351-360. 被引量:1

二级参考文献6

共引文献111

同被引文献4

引证文献1

二级引证文献7

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部