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淫羊藿苷抑制哮喘气道重塑和炎症反应。

Inhibition of airway remodeling and inflammatory response by Icariin in asthma.

机构信息

Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.

Institute of Integrated Traditional Chinese and Western Medicine, Huashan Hospital, Fudan University, Shanghai, China.

出版信息

BMC Complement Altern Med. 2019 Nov 19;19(1):316. doi: 10.1186/s12906-019-2743-x.

DOI:10.1186/s12906-019-2743-x
PMID:31744482
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6862818/
Abstract

BACKGROUND

Icariin (ICA) is the major active ingredient extracted from Chinese herbal medicine Epimedium, which has the effects of improving cardiovascular function, inducing tumor cell differentiation and increasing bone formation. It is still rarely reported that ICA can exert its therapeutic potential in asthma via anti-airway remodeling. The point of the study was to estimate the role of ICA in anti-. airway remodeling and its possible mechanism of action in a mouse ovalbumin. (OVA)-induced asthma model.

METHODS

Hematoxylin and Eosin Staining were performed for measuring airway remodeling related indicators. ELISA, Western blot and Immunohistochemistr-. y (IHC) were used for analyzing the level of protein. RT-PCR was used for analyzing the level of mRNA.

RESULTS

On days 1 and 8, mice were sensitized to OVA by intraperitoneal injection. From day 16 to day 43, previously sensitized mice were exposed to OVA once daily by nebulizer. Interventions were performed orally with ICA (ICA low, medium and high dose groups) or dexamethasone 1 h prior to each OVA exposure. ICA improves pulmonary function, attenuates pulmonary inflammation and airway remodeling in mice exposed to OVA. Histological and Western blot analysis of the lungs show that ICA suppressed transforming growth factor beta 1 and vascular endothelial growth factor expression. Increase in interleukin 13 and endothelin-1 in serum and bronchoalveolar lavage fluid in OVA-induced asthmatic mice are also decreased by ICA. ICA attenuates airway smooth muscle cell proliferation, as well as key factors in the MAPK/Erk pathway.

CONCLUSIONS

The fact that ICA can alleviate OVA-induced asthma at least partly through inhibition of ASMC proliferation via MAPK/Erk pathway provides a solid theoretical basis for ICA as a replacement therapy for asthma. These data reveal the underlying reasons of the use of ICA-rich herbs in Traditional Chinese Medicine to achieve good results in treating asthma.

摘要

背景

淫羊藿苷(ICA)是从中药淫羊藿中提取的主要活性成分,具有改善心血管功能、诱导肿瘤细胞分化和增加骨形成的作用。目前还很少有报道称 ICA 可以通过抗气道重塑发挥其在哮喘中的治疗潜力。本研究旨在评估 ICA 在卵清蛋白(OVA)诱导的哮喘小鼠模型中抗气道重塑的作用及其可能的作用机制。

方法

苏木精-伊红染色法测定气道重塑相关指标。酶联免疫吸附试验(ELISA)、Western blot 和免疫组织化学(IHC)用于分析蛋白水平。逆转录聚合酶链反应(RT-PCR)用于分析 mRNA 水平。

结果

第 1 天和第 8 天,通过腹腔注射对小鼠进行 OVA 致敏。从第 16 天到第 43 天,以前致敏的小鼠每天通过雾化器暴露于 OVA 一次。在每次 OVA 暴露前 1 小时,用 ICA(ICA 低、中、高剂量组)或地塞米松进行口服干预。ICA 改善了暴露于 OVA 的小鼠的肺功能,减轻了肺部炎症和气道重塑。肺组织学和 Western blot 分析显示,ICA 抑制了转化生长因子β 1 和血管内皮生长因子的表达。ICA 还降低了 OVA 诱导的哮喘小鼠血清和支气管肺泡灌洗液中白细胞介素 13 和内皮素-1 的水平。ICA 减弱了气道平滑肌细胞的增殖以及 MAPK/Erk 通路中的关键因子。

结论

ICA 通过 MAPK/Erk 通路抑制 ASMC 增殖至少部分缓解 OVA 诱导的哮喘的事实,为 ICA 作为哮喘替代疗法提供了坚实的理论基础。这些数据揭示了使用富含 ICA 的草药治疗哮喘取得良好效果的潜在原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcde/6862818/4250ba3c2f80/12906_2019_2743_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcde/6862818/3563dcf2e9db/12906_2019_2743_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcde/6862818/28685bab47a5/12906_2019_2743_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcde/6862818/174459e13fda/12906_2019_2743_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcde/6862818/267344b9d657/12906_2019_2743_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcde/6862818/4250ba3c2f80/12906_2019_2743_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcde/6862818/3563dcf2e9db/12906_2019_2743_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcde/6862818/28685bab47a5/12906_2019_2743_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcde/6862818/174459e13fda/12906_2019_2743_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcde/6862818/267344b9d657/12906_2019_2743_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcde/6862818/4250ba3c2f80/12906_2019_2743_Fig5_HTML.jpg

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