iTRAQ-Based Proteomics Reveals Gu-Ben-Fang-Xiao Decoction Alleviates Airway Remodeling via Reducing Extracellular Matrix Deposition in a Murine Model of Chronic Remission Asthma.
iTRAQ-Based Proteomics Reveals Gu-Ben-Fang-Xiao Decoction Alleviates Airway Remodeling via Reducing Extracellular Matrix Deposition in a Murine Model of Chronic Remission Asthma.
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基于 iTRAQ 的蛋白质组学揭示固本防笑汤通过减少慢性缓解哮喘小鼠模型中的细胞外基质沉积来减轻气道重塑
DOI：
10.3389/fphar.2021.588588
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发表时间：
2021
影响因子：
5.6
通讯作者：
Hou S
中科院分区：
文献类型：
--
作者：
Xing Q;You Y;Zhao X;Ji J;Yan H;Dong Y;Ren L;Ding Y;Hou S
气道重塑是哮喘的主要病理特征。目前哮喘的治疗主要针对减轻炎症，但不是特别针对气道重塑。因此，值得开发替代和更有效的治疗方法来减轻重塑。固本防哮汤治疗哮喘已有数十年的历史。在本研究中，GBFXD调节慢性缓解哮喘（CRA）小鼠模型的气道炎症、胶原沉积以及与气道重塑相关的分子如波形蛋白、α-SMA、羟脯氨酸和E-cadherin。蛋白质组学分析表明，重叠的差异表达蛋白（DEP）（模型/对照和GBFXD/模型）主要是胶原和层粘连蛋白，这是细胞外基质（ECM）蛋白。此外，KEGG分析表明，GBFXD可以调节与气道重塑相关的途径，包括ECM-受体相互作用、粘着斑和PI 3 K/AKT信号通路，这是模型/对照和GBFXD/模型中含有最多DEP的前三个显著富集的途径。进一步的验证研究表明，GBFXD调节reticulon-4（RTN 4）并抑制PI 3 K/AKT通路的激活，以减轻ECM蛋白沉积。本研究结果提示，GBFXD可能通过RTN 4调节PI 3 K/AKT通路改善气道重塑，为进一步研究GBFXD治疗CRA的分子机制提供了新的思路。
Airway remodeling is a primary pathological feature of asthma. The current therapy for asthma mainly targets reducing inflammation but not particularly airway remodeling. Therefore, it is worthwhile to develop alternative and more effective therapies to attenuate remodeling. Gu-Ben-Fang-Xiao Decoction (GBFXD) has been used to effectively and safely treat asthma for decades. In this study, GBFXD regulated airway inflammation, collagen deposition, and the molecules relevant to airway remodeling such as Vimentin, α-SMA, hydroxyproline, and E-cadherin in chronic remission asthma (CRA) murine model. Proteomic analysis indicated that the overlapping differentially expressed proteins (DEPs) (Model/Control and GBFXD/Model) were mainly collagens and laminins, which were extracellular matrix (ECM) proteins. In addition, the KEGG analysis showed that GBFXD could regulate pathways related to airway remodeling including ECM-receptor interactions, focal adhesion, and the PI3K/AKT signaling pathway, which were the top three significantly enriched pathways containing the most DEPs for both Model/Control and GBFXD/Model. Further validation research showed that GBFXD regulated reticulon-4 (RTN4) and suppressed the activation of the PI3K/AKT pathway to alleviate ECM proteins deposition. In conclusion, our findings indicate that GBFXD possibly regulate the PI3K/AKT pathway via RTN4 to improve airway remodeling, which provides a new insight into the molecular mechanism of GBFXD for the treatment of CRA.
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影响因子：
24.3
作者：
Baraldo, S.;Turato, G.;Saetta, M.
通讯作者：
Saetta, M.
DOI：
10.1164/rccm.201810-1855oc
发表时间：
2019-08-15
影响因子：
24.7
作者：
Mostaco-Guidolin, Leila B.;Osei, Emmanuel T.;Hackett, Tillie-Louise
通讯作者：
Hackett, Tillie-Louise
影响因子：
5.8
作者：
Halwani R;Sultana A;Al-Kufaidy R;Jamhawi A;Vazquez-Tello A;Al-Muhsen S
通讯作者：
Al-Muhsen S
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
影响因子：
7.5
作者：
Cui, Jie;Xu, Fei;Dong, Jingcheng
通讯作者：
Dong, Jingcheng
影响因子：
14.2
作者：
Lazarinis, Nikolaos;Bood, Johan;Dahlen, Barbro
通讯作者：
Dahlen, Barbro