文章摘要
袁为远,魏盼,包凯帆,姚露,王霄彤,王思齐,郑劼,洪敏,江国荣.麻黄-甘草药对抑制过敏性哮喘的效应及机制初探[J].南京中医药大学学报(社会科学版),2020,36(1):41-45.
麻黄-甘草药对抑制过敏性哮喘的效应及机制初探
Effects and Mechanism of Mahuang-Gancao Couplet Medicines on Allergic Asthma
  
DOI:
中文关键词: 关键词:麻黄-甘草药对  上皮间质转化  气道重塑  过敏性哮喘
英文关键词: Mahuang-Gancao couplet medicines  epithelial-mesenchymal transition  airway remodeling  allergic asthma
基金项目:
作者单位
袁为远1,2,3,魏盼1,2,3,包凯帆1,2,姚露1,2,王霄彤1,2,王思齐1,2,郑劼4,洪敏1,2,江国荣3 1.南京中医药大学药学院江苏 南京 2100232.江苏省中药药效与安全评价重点实验室江苏 南京 2100233.南京中医药大学附属苏州市中医医院江苏 苏州 2150034.南京中医药大学医学院·整合医学学院江苏 南京 210023 
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中文摘要:
      目的 研究麻黄-甘草药对对过敏性哮喘的影响,并初步探讨其作用机制。方法 建立屋尘螨(HDM)诱导的过敏性哮喘模型,造模同时给予麻黄-甘草药对提取物(MG)。使用无创肺功能仪检测小鼠气道反应性,HE染色观察小鼠肺组织病理学变化,Masson染色观察小鼠肺组织的胶原沉积情况,进行血液嗜酸性粒细胞(EOS)计数,ELISA法检测支气管肺泡灌洗液(BALF)及肺组织IL-4、IL-5、IL-13、TGF-β1及血清IgE的表达,免疫组化检测肺组织E-cadherin、N-cadherin、Vimentin、α-SMA和TGF-β1蛋白表达情况。结果 MG可显著降低气道高反应性,抑制BALF及肺组织IL-4、IL-5和IL-13的表达,降低血液EOS及血清IgE的表达,并且减轻肺组织的炎症浸润及胶原沉积。进一步结果表明MG可抑制肺组织TGF-β1的表达,上调E-cadherin以及下调N-cadherin、Vimentin、α-SMA的表达。结论 MG能够通过抑制支气管上皮间质转化,从而缓解气道的炎症状态以及改善哮喘的气道重塑,进而发挥对过敏性哮喘的治疗作用。
英文摘要:
      OBJECTIVE To investigate the effect and mechanism of Mahuang-Gancao couplet medicines (MG) on allergic asthma. METHODS The airway responsiveness was detected by non-invasive pulmonary function test. The pathological changes of lung tissue were observed by HE staining. The collagen deposition of lung tissue was observed by Masson staining. The eosinophil (EOS) count in blood was performed. IL-4, IL-5, IL-13, TGF-β1 and IgE were detected by ELISA assay. The expression of E-cadherin, N-cadherin, Vimentin, α-SMA and TGF-β1 were detected by immunohistochemistry. RESULTS MG significantly reduced airway hyperresponsiveness, inhibited the expression of IL-4, IL-5 and IL-13 in BALF and lung tissue, decreased the expression of serum IgE, and alleviated inflammation of lung tissue. MG inhibited the expression of TGF-β1 in lung tissue, increased the expression of E-cadherin and down-regulated the expression of N-cadherin, Vimentin and α-SMA. CONCLUSION MG can play a key role in the treatment of allergic asthma by inhibiting the bronchial epithelial-mesenchymal transition, thereby alleviating the inflammatory state of the airway and improving the airway remodeling of asthma.
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