期刊文献+

CVA模型大鼠痰瘀同治气道炎症TGF-β1、IL-13、VEGF及NF-κB之间的相关性研究 被引量:6

Correlative Study Between Airway Inflammation and Serum TGF-β1,IL-13,VEGF,NF-κB in Rats with CVA by Phlegm and Blood Stasis Stagnation
下载PDF
导出
摘要 目的:探讨痰瘀同治CVA模型大鼠气道炎症及其与TGF-β1、IL-13、VEGF及NF-κB之间的相关性,为从痰瘀论治小儿CVA提供理论支持。方法:雌性SPF级大鼠72只随机分为正常对照组、模型组、辅舒酮组、健脾化痰组、行气化瘀组、痰瘀同治组,每组12只。造模30天后,正常对照组、模型组每天给予生理盐水灌胃,各治疗组给予相应药物灌胃,干预30后取材,观察各组大鼠气道炎症情况并测定血清中TGF-β1、IL-13、VEGF及NF-κB水平。结果:正常对照组大鼠无明显炎症细胞浸润,模型组大鼠支气管周围炎症细胞浸润明显,以嗜酸性粒细胞和淋巴细胞浸润为主,浸润程度明显高于正常对照组(P<0.05);药物干预后大鼠肺组织炎症细胞浸润程度明显减轻,且以痰瘀同治组更明显(P<0.05)。大鼠血清中TGF-β1、IL-13、VEGF及NF-κB的表达水平,模型组显著高于正常对照组(P<0.05);药物干预可抑制TGF-β1、IL-13、VEGF及NF-κB的表达,且痰瘀同治组改善效果更明显(P<0.05)。嗜酸性粒细胞浸润与TGF-β1、IL-13、VEGF及NF-κB表达呈正相关关系(P<0.05)。结论:TGF-β1、IL-13、VEGF及NF-κB在CVA大鼠过度表达,这些因子与CVA气道炎症有很好相关性,痰瘀同治法可抑制这些因子活性,从而减轻和控制CVA气道炎症的作用。 Objective: To investigate the phlegm and blood stasis pathogenesis on airway inflammation in cough variant asthma(CVA) model rats and the correlation between airway inflammation and transforming growth factor- β1 (TGF- β1 ), interleukin - 13 ( IL - 13 ), vascular endothelial growth factor( VEGF), nuclear factor kappa - B ( NF - κB ), provide theoretical support for the treatment of children with CVA. Methods : 72 female SPF rats were randomly divided into a normal control group, a model group, a Flixotide group, a phlegm - reducing group, a blood - stasis dispersing group, a phlegm and blood stasis stagnation treatment group, with 12 in each group. Building models after 30 days, and normal control group and model group was lavaged by saline every day, each treatment group were given drug lavage, materials after intervention for 30 days. Observe airway inflammation of rats in each group and the level of serum TGF - β1, IL - 13, VEGF and NF - κB. Results: The rats in normal control group had no obvious inflammatory cell infiltration. Inflammation cell infiltration was significant around bronchial of rats in the model group, mainly eosinophils and lymphocyte. Infiltration degree was significantly higher than that in normal control group (P 〈 0.05 ) ; inflammation cells infiltration reduced significantly in rats' lung tissue after drug intervention, and the phlegm and blood stasis stagnation treatment group was more obvious ( P 〈 0. 05 ). The expressions of TGF - β1, IL - 13, VEGF and NF - κB were significantly higher than those of normal control group (P 〈 0. 05 ) ;the drug intervention could inhibit the expressions of TGF - β1, IL - 13, VEGF and NF - κB, and the effect was more obvious in phlegm and blood stasis stagnation treatment group (P 〈 0.05 ). Eosinophils infiltration was positively related to TGFβ1, IL - 13, VEGF and NF - κB (P 〈 0.05 ). Conclusion: The expressions of TGF - β1, IL - 13, VEGF and NF - κB are excessive in CVA rats. These factors have a good correlation with CVA airway inflammation. The phlegm and blood stasis treatment can restrain activity of these factors, so as to reduce and control the CVA airway inflammation.
作者 李冬梅 施雷 王文丽 LI Dong - mei SHI Lei WANG Wen - li(The Affiliated Hospital of Liaoning University of TCM, Shenyang 110032, China TCM Hospital of Huanggu District ,Shenyang 110032, China)
出处 《中医药学报》 CAS 2016年第6期37-41,共5页 Acta Chinese Medicine and Pharmacology
基金 沈阳市科技创新专项资金-人口与健康科技公关专项(F14-158-9-09)
关键词 痰瘀同治 咳嗽变异性哮喘模型 气道炎症 转化生长因子-β1 白介素-13 血管内皮生长因子 转录因子蛋白 相关性 Treatment of phlegm and blood stasis stagnation Cough variant asthma model Airway inflammation Trans-forming growth factor -β1 Interleukin - 13 Vascular endothelial growth factor Nuclear factor kappa - B Correlation
  • 相关文献

参考文献10

二级参考文献81

  • 1王立波.人类T_H细胞亚群与支气管哮喘[J].国外医学(免疫学分册),1995,18(1):21-23. 被引量:14
  • 2中华医学会呼吸病学分会哮喘学组.咳嗽的诊断与治疗指南(草案)[J].中华结核和呼吸杂志,2005,28(11):738-744. 被引量:1456
  • 3赖克方.咳嗽严重度界定与咳嗽激发试验[J].中国实用内科杂志,2006,26(1):15-17. 被引量:95
  • 4中华医学会呼吸病学分会哮喘学组.哮喘诊治指南(2007年修订版).中华结核和呼吸杂志,2007,30(1):8-8.
  • 5俞森洋.呼吸内科主治医师660问[M].2版.北京:中国协和医科大学出版社,2009:245-246.
  • 6Nattson MP, Camandola S. NF -кB in neuronal plasticity and neurodegenerative disordersl[J]. J Clin Invest, 2001, 107(3): 247-254.
  • 7Kaltschmidt B, Uherek M, Wellmann H, et al. Inhibition of NF- кB potentiates amyloid beta- mediated neuronal apoptosis[J]. Proc Natl Acad Sci USA, 1999,96(16):9409-9414.
  • 8Yamamoto Y, Gaynor RB. Therapeutic potential of inhibition of the NF- kappaB pathway in the treatment of inflammation and cancer[J]. J Clin Invest, 2001,107(2) : 135 - 142.
  • 9Rossi A. Anti- inflammatory cyclopentenone prostagtandins are direct inhibitors of IкB kinase [ J]. Nature, 2000, 403(6765) : 103 - 108.
  • 10Adams J. Proteasome inhibitors: a novel class of potent and effective antiuunor agents[J]. Cancer Res, 1999, 59(11):2615 - 2622.

共引文献189

同被引文献85

引证文献6

二级引证文献53

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