期刊文献+

二黄汤对哮喘模型大鼠肺组织中TGF-β_1及体内IL-33的影响 被引量:2

The Effect of Erhuang Decoction on Transforming Growth Factor-β_1 of Lung Tissues and the Expression of Leukotriene-33 in Asthmatic Rats
下载PDF
导出
摘要 目的观察二黄汤对哮喘模型大鼠肺组织中转化生长因子β1(TGF-β1)及体内白介素-33(IL-33)的影响。方法 50只SD大鼠随机均分为正常组、哮喘组、布地奈德组、高剂量二黄汤组(含生药量68 g/kg)和低剂量二黄汤组(含生药量17 g/kg)。以卵清白蛋白致敏与激发建立哮喘大鼠模型,随后分别用布地奈德、二黄汤干预治疗。肺组织切片HE染色观察病理变化并检测气道管壁厚度(Wat)及气道平滑肌厚度(Wam),用免疫组化法检测肺组织TGF-β1蛋白的表达,酶联免疫法检测血清及支气管肺泡灌洗液(BALF)中IL-33的含量。结果所有药物干预组较哮喘组炎症细胞浸润明显减轻;布地奈德组、高剂量二黄汤组和低剂量二黄汤组Wat均较哮喘组下降(μm2/μm:54.99±8.82、52.28±7.61、58.53±7.63 vs 79.50±5.64,P<0.05);布地奈德组、高剂量二黄汤组和低剂量二黄汤组Wam均较哮喘组下降(μm2/μm:22.74±2.73、20.63±1.72、21.20±4.50 vs 30.16±1.68,P<0.05);与正常组比较,哮喘组BALF、血清中IL-33的浓度增高,经药物干预后,布地奈德组、高剂量二黄汤组和低剂量二黄汤组低于哮喘组(P<0.05),但3干预组间差异无统计学意义;哮喘组TGF-β1高于正常组(IOD:12.60±2.25 vs 1.67±0.17),布地奈德组(5.51±2.48)、高剂量二黄汤组(5.22±2.52)和低剂量二黄汤组(6.92±2.18)均低于哮喘组(P<0.05),3干预组间差异无统计学意义。哮喘大鼠的气道壁厚度和平滑肌厚度与TGF-β1、IL-33呈正相关。结论二黄汤可在一定程度上干预哮喘大鼠气道重塑,其作用可能是通过调节TGF-β1和IL-33实现的。 Objective To investigate the effect of Erhuang decoction on TGF-β1 expression of lung tiusses and the concentrations of IL-33 in asthmatic rats. Methods Fifty Sprague-Dawley rats were randomly divided into five groups equally:Control group, Asthmatic group, Budesonide aerosol group, High-dose Erhuang decoction group ( 68 g/kg)and Low-dose Erhuang decoction group(17 g/kg). The model of asthma was established by ovalbumin (OVA) sensitizing and challeng-ing. Then Erhuang decoction and budesonide aerosol was used respectively for intervention therapy. Histologic HE staining were used to observe the general pathologic alteration and to analyze the total bronchial wall area (Wat) and the muscle wall area(Wam). The protein expressions of TGF-β1 in the lung tissues were detected by immunohistochemistry. The concentra-tions serum IL-33 and BALF were tested by sandwich ELISA. Results There was significant reduction in the infiltrated inflammatory cells in all drug intervention groups compared with asthma group;The Wat and Wam in asthmatic group was significantly higher in than those in Budesonide aerosol group,High-dose Erhuang decoction group and Low-dose Erhuang decoction group ( Watμm2/μm:54.99±8.82, 52.28±7.61, 58.53±7.63 vs 79.50±5.64, P&lt;0.05;Wamμm2/μm:22.74±2.73, 20.63±1.72, 21.20±4.50 vs 30.16±1.68, P&lt;0.05);Compared with control group, BALF and serum IL-33 concentration were significantly higher in asthmatic group. Compared with asthmatic group, all the indicators were significantly decrease in the treatment groups after drug intervention (P&lt;0.05). Andthere was no significant difference between the treatment groups in all the indicators. TGF-β1 expression in lung tissues in asthmatic group were significantly higher than that in control group (12.60 ± 2.25 vs 1.67 ± 0.17). Compared with asthmatic group, there was significantly reduction of TGF-β1 expression in the Budesonide aerosol group (5.51±2.48), High-dose Erhuang decoction group (5.22±2.52) and Low-dose Erhuang decoction group (6.92 ±2.18) (P&lt;0.05). There were no significant difference between the treatment groups. TGF-β1 expression and se-rum IL-33 concentration in asthmatic rats were positively correlated with Wat and Wam. Conclusion The effects of Er-huang decotion on ameliorating the progression of airway remodeling about asthmatic rats may be partially by regulating TGF-β1 and IL-33.
出处 《天津医药》 CAS 北大核心 2014年第4期337-340,共4页 Tianjin Medical Journal
  • 相关文献

参考文献11

二级参考文献42

  • 1倪健,董竞成.三种中药药效成分抗支气管哮喘变应性炎症的实验研究[J].中国实验方剂学杂志,2004,10(4):49-51. 被引量:41
  • 2王光辉,金发光,楚东岭,段丽.哮喘豚鼠气道重构中基质金属蛋白酶-9及抑制物TIMP-1的表达[J].第四军医大学学报,2006,27(14):1259-1262. 被引量:9
  • 3许淑云,徐永健,张珍祥,倪望,陈士新.支气管哮喘模型大鼠气道重建的特征及机制[J].华中科技大学学报(医学版),2006,35(4):465-468. 被引量:16
  • 4管小俊,张维溪,李昌崇,郑仰明,林立,叶乐平,陈小芳,罗运春,蔡晓红,董琳,张海邻,周晓聪.细胞外信号调节激酶和转化生长因子β1在哮喘气道重塑中的作用以及糖皮质激素的调控[J].中华医学杂志,2007,87(25):1767-1772. 被引量:33
  • 5HOLGATE S T,PETERS-GOIDEN M,JPANETTIERI R A,et al.Roles of cysteinyl leukotrienes in airway inflammation,smooth muscle[unction,and remodeling[J].J Allergy Clin Immunol,2003,111(Suppl.1):S18-S34.
  • 6VIGNOLA A M,RICCOBONO L,MIRABELLA A,et al.Sputum metalloproteinase-9/tissue inhibitor of metalloproteinase-1 ratio correlates with airflow obstruction in asthma and chronic bronchitis[J].Am J Respir Crit Care Med,1998,158(6):1945-1950.
  • 7CATALDO D D,TOURNOY K G,VERMAELEN K,et al.Matrix metalloproteinase-9 deficiency impairs cellular infilatration and bronchial hyperresponsiveness during allergen induced airway inflammation[J].Am J Pathol,2002,161(2):491-498.
  • 8PALMANS E,KIPS J C,PAUMWELS R A.Prolonged allergen exposure induces structural airway changes in sensitized rats[J].Am J Respir Crit Care Med,2000,161 (2 Pt 1):627-635.
  • 9HOSHINO M,TAKEHASHI M,TAKAI Y,et al.Inhaled corticosteroids decrease subepithelial collagen deposition by modulation of lhe balance between matrix metalloproteinase-9 and inhibitor of metalloproteinase-1 expression in asthma[J].J Allergy Clin Immunol,1999,104(2 Pt 1):356-363.
  • 10Bahadori K,Doyle-Waters MM,Marra C,et al.Economic burden of asthmas a systematic review.BMC Pulm.Med,2009,9:24.

共引文献28

同被引文献36

  • 1李志平,钟韵,郭禹标,彭丽红,黄旭斌,黄建强,谢灿茂.支气管哮喘患者抑郁情绪、哮喘控制及生存质量的调查分析[J].实用医学杂志,2007,23(5):745-746. 被引量:10
  • 2Yadav UC, Naura AS, Aguilera-Aguirre L,et al. Aldosereductase in hibition prevents allergic airway remodeling throughPI3K/AKT/GSK33 pathway in mice [J]. PLoS One, 2013,8(2):e57442.
  • 3Vittal R, Mickler EA, Fisher AJ, et al.Type V collagen inducedtolerance suppresses collagen deposition, TGF-pand associatedtranscripts in pulmonary fibrosis [J]. PLoS One,2013,8 (10):e76451.
  • 4Haczku A, Panettieri RA. Social stress and asthma: the role ofcorticosteroid insensitivity [J]. J Allergy Clin Immunol,2010,125(3):550-558.
  • 5Rilz T, steptoe A, DeWilde S, et al. Emotions and stressincrease respiratory resistance in asthma [J]. PsychosomMed, 2000,62(3): 401-412.
  • 6Bottoms SE, Howell JE, Reinhardt AK, et al. Tgf-Beta isoformspecific regulation of airway inflammation and remodeling in amurine model of asthma [J]. PLoS One, 2010,5(3) :e9674.
  • 7Pemg DW, Chang KT,Su KC, et al. Matrix metaUoprotease-9induces transform-ing growth factor-p ( 1 ) production in airwayepithelium via activation of epi-dermal growth factor receptors[J]. Life Sci, 2011, 89(5-6):204-212.
  • 8Hosoki K, Kainuma K, Toda M , et al. Montelukast suppressesepithelial to mesen-chymal transition of bronchial epithelial cellsinduced by eosinophils [J]. Biochem Biophy Res Commun,2014,449(3):351-356.
  • 9Kamekura R, Kojima T, Takano K, et al.The role of IL-33 and its re- ceptor ST2 in human nasal epithelium with allergic rhinitis[J].Clin Exp Allergy, 2012, 42(2):218- 228. doi: 10.1111/j.1365- 2222.2011.03867.x.
  • 10Nakae S, Morita H, Ohno T, et al. Role of interleukin-33 in innate- type immune ceils in allergy[J]. Allergol Int, 2013, 62(1):13-20. doi: 10.2332/allergolint.13-RAI-0538.

引证文献2

二级引证文献6

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