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温通汤通过调节嗜酸性粒细胞凋亡失衡来治疗过敏性支气管哮喘。

Wentong decoction cures allergic bronchial asthma by regulating the apoptosis imbalance of EOS.

作者信息

Yan Yue, Bao Hai-Peng, Li Chun-Lei, Shi Qi, Kong Yan-Hua, Yao Ting, Li You-Lin

机构信息

1The 2nd Department of Pulmonary Disease in TCM, The Key Unit of SATCM Pneumonopathy Chronic Cough and Dyspnea, Beijing Key Laboratory of Prevention and Treatment of Allergic Diseases With TCM (No. BZ0321), Center of Respiratory Medicine, China-Japan Friendship Hospital, National Clinical Research Center for Respiratory Diseases, Beijing, 100029 China.

2Beijing University of Chinese Medicine, Beijing, 100029 China.

出版信息

Chin Med. 2018 Apr 18;13:21. doi: 10.1186/s13020-018-0180-2. eCollection 2018.

DOI:10.1186/s13020-018-0180-2
PMID:29713367
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5907368/
Abstract

BACKGROUND

Eosinophils (EOS) is one of the most important cells involved in the pathogenesis of chronic airway inflammation in asthma, and its apoptosis is part of the mechanisms of asthma. Therefore, this study aimed to observe the effect of Chinese medicine Wentong decoction (WTD) in EOS apoptosis in asthmatic rats. This work also explored the mechanism of WTD regulation in EOS apoptosis and provided a new target for clinical treatment of asthma.

METHODS

Asthmatic rats induced by ovalbumin were treated with WTD. Lung function of rats in each group was detected, and lung tissue pathology, EOS counts in blood and bronchoalveolar lavage fluid were observed. The degree of the EOS apoptosis in rats was detected. The expression content of interleukin (IL)-5, IL-10, chemokine (C-C motif) ligand 5 (CCL5), granulocyte-macrophage colony-stimulating factor (GM-CSF), transforming growth factor beta 1 (TGF-β1), interferon (IFN)-γ, and other cytokines in rat serum and the genes of Eotaxin mRNA, Fas mRNA, FasL mRNA, Fas/FasL and Bcl-2 mRNA in the lung tissues were determined.

RESULTS

WTD can reduced airway resistance in rat models and improved airway compliance. The pathological changes of lung tissue in WTD group were significantly alleviated, at the same time, WTD could reduce the EOS count in the blood and BALF smears of the asthmatic model rats. Compared with the model group, the apoptosis degree of EOS significantly increased in rats in the WTD group. The expression of IL-5, CCL5, and GM-CSF in the serum and the expression of Eotaxin mRNA, Bcl-2 mRNA in the lung tissues in rats in the WTD group rats decreased. Moreover, the expression of IL-10, TGF-β1, and IFN-γ in the serum and the expression of Fas mRNA, FasL mRNA in the lung tissues in rats in the WTD group rats increased compared with that in rats in the model group.

CONCLUSIONS

Wentong decoction may accelerate EOS apoptosis, reduce asthma inflammation, and alleviate the disease through regulating and controlling the factors related to the anti-apoptosis and pro-apoptosis.

摘要

背景

嗜酸性粒细胞(EOS)是参与哮喘慢性气道炎症发病机制的最重要细胞之一,其凋亡是哮喘发病机制的一部分。因此,本研究旨在观察中药温通方(WTD)对哮喘大鼠EOS凋亡的影响。本研究还探讨了WTD调节EOS凋亡的机制,为哮喘的临床治疗提供新靶点。

方法

用卵清蛋白诱导哮喘大鼠,并用WTD治疗。检测各组大鼠的肺功能,观察肺组织病理学、血液及支气管肺泡灌洗液中的EOS计数。检测大鼠EOS凋亡程度。测定大鼠血清中白细胞介素(IL)-5、IL-10、趋化因子(C-C基序)配体5(CCL5)、粒细胞-巨噬细胞集落刺激因子(GM-CSF)、转化生长因子β1(TGF-β1)、干扰素(IFN)-γ等细胞因子的表达含量以及肺组织中嗜酸性粒细胞趋化因子mRNA、Fas mRNA、FasL mRNA、Fas/FasL和Bcl-2 mRNA的基因。

结果

WTD可降低大鼠模型的气道阻力,改善气道顺应性。WTD组肺组织病理变化明显减轻,同时,WTD可降低哮喘模型大鼠血液和BALF涂片中的EOS计数。与模型组相比,WTD组大鼠EOS凋亡程度显著增加。WTD组大鼠血清中IL-5、CCL5和GM-CSF的表达以及肺组织中嗜酸性粒细胞趋化因子mRNA、Bcl-2 mRNA的表达降低。此外,与模型组大鼠相比,WTD组大鼠血清中IL-10、TGF-β1和IFN-γ的表达以及肺组织中Fas mRNA、FasL mRNA的表达增加。

结论

温通方可能通过调控与抗凋亡和促凋亡相关的因子,加速EOS凋亡,减轻哮喘炎症,缓解病情。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/a0276338b59c/13020_2018_180_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/d1466f674ae0/13020_2018_180_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/4a2a44185791/13020_2018_180_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/ce27d4a6cf47/13020_2018_180_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/dbf13d42b418/13020_2018_180_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/9247749012e5/13020_2018_180_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/a0276338b59c/13020_2018_180_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/d1466f674ae0/13020_2018_180_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/4a2a44185791/13020_2018_180_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/ce27d4a6cf47/13020_2018_180_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/dbf13d42b418/13020_2018_180_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/9247749012e5/13020_2018_180_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2355/5907368/a0276338b59c/13020_2018_180_Fig6_HTML.jpg

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