Osthole attenuates asthma-induced airway epithelial cell apoptosis and inflammation by suppressing TSLP/NF-κB-mediated inhibition of Th2 differentiation.

IF 2.6 4区医学 Q2 ALLERGY

Allergy Asthma and Clinical Immunology Pub Date : 2024-09-27 DOI:10.1186/s13223-024-00913-8

Yanli Li, Yushan Zhou, Liqiong Liu, Yunfeng Yang, Yanhong Liu, Dailing Yan, Juyan Chen, Yi Xiao

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引用次数: 0

Abstract

Objective: The aim of this study was to investigate the influence of osthole (OS) on asthma-induced airway epithelial cell apoptosis and inflammation by restraining Th2 differentiation through suppressing TSLP/NF-κB.

Methods: An asthma mouse model and an inflammation cell model were constructed with ovalbumin (OVA) and lipopolysaccharide (LPS), respectively. CD4 + T cells were treated with IL-4 to induce Th2 differentiation. Model mice were treated with OS (15,40 mg/kg) for 7 days, and 10 µg/mL OS was added to cell treatment groups. The levels of relevant indices were detected by RT‒qPCR, HE and Masson staining, Western blotting, ELISA and flow cytometry.

Results: In a mouse asthma model, TSLP expression was elevated, and the NF-κB pathway was activated. Therefore, OS could restrain the apoptosis and inflammation of airway epithelial cells. Downstream mechanistic studies revealed that OS can suppress Th2 differentiation by restraining the level of TSLP and NF-κB nuclear translocation, thus facilitating the proliferation of airway epithelial cells, restraining their apoptosis and inflammation, and alleviating airway inflammation in asthmatic mice.

Conclusion: OS can inhibit Th2 differentiation by inhibiting the TSLP and NF-κB pathways, which can reduce the apoptosis and inflammation of airway epithelial cells caused by asthma.

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Osthole通过抑制TSLP/NF-κB介导的Th2分化抑制作用，减轻哮喘诱导的气道上皮细胞凋亡和炎症。

研究目的本研究的目的是通过抑制TSLP/NF-κB抑制Th2分化，研究osthole（OS）对哮喘诱导的气道上皮细胞凋亡和炎症的影响：方法：分别用卵清蛋白（OVA）和脂多糖（LPS）构建哮喘小鼠模型和炎症细胞模型。用 IL-4 处理 CD4 + T 细胞以诱导 Th2 分化。用 OS（15、40 毫克/千克）治疗模型小鼠 7 天，并在细胞治疗组中加入 10 微克/毫升 OS。通过 RT-qPCR、HE 和 Masson 染色、Western 印迹、ELISA 和流式细胞术检测相关指标的水平：结果：在小鼠哮喘模型中，TSLP表达升高，NF-κB通路被激活。因此，OS 能抑制气道上皮细胞的凋亡和炎症反应。下游机理研究发现，OS可通过抑制TSLP水平和NF-κB核转位来抑制Th2分化，从而促进气道上皮细胞增殖，抑制其凋亡和炎症，缓解哮喘小鼠的气道炎症：结论：OS能通过抑制TSLP和NF-κB通路抑制Th2分化，从而减少哮喘引起的气道上皮细胞凋亡和炎症。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Allergy Asthma and Clinical Immunology ALLERGY-IMMUNOLOGY

CiteScore

4.30

自引率

3.70%

发文量

审稿时长

12 weeks

期刊介绍： Allergy, Asthma & Clinical Immunology (AACI), the official journal of the Canadian Society of Allergy and Clinical Immunology (CSACI), is an open access journal that encompasses all aspects of diagnosis, epidemiology, prevention and treatment of allergic and immunologic disease. By offering a high-visibility forum for new insights and discussions, AACI provides a platform for the dissemination of allergy and clinical immunology research and reviews amongst allergists, pulmonologists, immunologists and other physicians, healthcare workers, medical students and the public worldwide. AACI reports on basic research and clinically applied studies in the following areas and other related topics: asthma and occupational lung disease, rhinoconjunctivitis and rhinosinusitis, drug hypersensitivity, allergic skin diseases, urticaria and angioedema, venom hypersensitivity, anaphylaxis and food allergy, immunotherapy, immune modulators and biologics, immune deficiency and autoimmunity, T cell and B cell functions, regulatory T cells, natural killer cells, mast cell and eosinophil functions, complement abnormalities.