Bu-Shen-Yi-Qi formula ameliorates airway remodeling in murine chronic asthma by modulating airway inflammation and oxidative stress in the lung
Bu-Shen-Yi-Qi formula ameliorates airway remodeling in murine chronic asthma by modulating airway inflammation and oxidative stress in the lung
复制标题
补肾益气方通过调节气道炎症和肺部氧化应激改善小鼠慢性哮喘气道重塑
DOI：
10.1016/j.biopha.2019.108694
复制
发表时间：
2019-04-01
影响因子：
7.5
通讯作者：
Dong, Jingcheng
中科院分区：
文献类型：
--
作者：
Cui, Jie;Xu, Fei;Dong, Jingcheng
补肾益气方对慢性气道炎症有一定的抑制作用。然而，BSYQF治疗慢性哮喘气道重塑的直接实验证据相对较少。最近的证据表明，氧化应激参与气道炎症和气道重塑在慢性哮喘。BSYQF含有多种具有抗氧化作用的化学成分，可能有利于减轻慢性哮喘气道重塑。本研究的目的是阐明BSYQF治疗对慢性哮喘气道重塑的影响，并探讨其潜在机制。为了建立慢性哮喘小鼠模型，BALB/c小鼠对卵清蛋白致敏和刺激8周。分别口服BSYQF（5、10、20 g生药/kg体重）或噻托溴铵（0.1 mM）。观察BSYQF对肺炎症和肺重构的影响。分析大鼠肺组织氧化应激参数。BSYQF治疗可降低气道高反应性（AHR）、Th2反应（包括IL-4、IL-13、ova特异性IgE和IgG1）、转化生长因子- β (tgf - β)、血管内皮生长因子（VEGF）、气道炎症和气道重塑（包括平滑肌增厚和支气管周围胶原沉积）。在氧化应激方面，BSYQF处理可降低大鼠肺组织活性氧（ROS）、丙二醛（MDA）、NO及诱导型一氧化氮合酶（iNOS）表达，显著升高肺组织谷胱甘肽(GSH) /氧化谷胱甘肽（GSSH）比值，恢复支气管上皮线粒体超微结构变化及肺组织ATP水平。综上所述，本研究提示BSYQF治疗可改善慢性哮喘模型气道重塑，减轻哮喘特征。BSYQF的抗炎和抗氧化作用可能解释了为什么BSYQF具有防止气道重塑的作用。
Bu-Shen-Yi-Qi formula (BSYQF) could suppress chronic airway inflammation according to previous studies. However, there is relatively little direct experimental evidence to evaluate the effects of BSYQF treatment on airway remodeling in chronic asthma. Recent evidence suggests that oxidative stress is involved in airway inflammation and airway remodeling in chronic asthma. BSYQF which includes various of chemical components having antioxidant effects, could be beneficial in attenuating airway remodeling in chronic asthma. The purpose of this study was to elucidate the effect of BSYQF treatment on airway remodeling and investigate its potential mechanisms in chronic asthma. To develop the murine models of chronic asthma, BALB/c mice were sensitized and challenged to ovalbumin for 8 weeks. BSYQF (5, 10, 20 g raw herbs/kg body weight) or tiotropium bromide (0.1 mM) were administered orally and intranasal instillation, respectively. The effect of BSYQF on pulmonary inflammation and remodeling was evaluated. The parameters of oxidative stress in the lung were analyzed. BSYQF treatment reduced airway hyperresponsiveness (AHR), Th2 response including IL-4, IL-13, and OVA-specific IgE and IgG1, transforming growth factor-beta (TGF-beta), vascular endothelium growth factor (VEGF), airway inflammation and airway remodeling including smooth muscle thickening and peribronchial collagen deposition. As for oxidative stress, BSYQF treatment reduced reactive oxygen species (ROS), Malondialdehyde (MDA), NO, and the expression of inducible nitric oxide synthase (iNOS), but increased significantly glutathione (GSH) /Oxidized glutathione(GSSH) ratios in the lung, restored mitochondrial ultrastructural changes of bronchial epithelia and ATP levels in the lung.In summary, this study suggested that BSYQF treatment ameliorated airway remodeling and alleviated asthmatic features in chronic asthma models. Anti-inflammatory and antioxidant effect of BSYQF may explain why BSYQF has effects on preventing airway remodeling.