Compound D from Zingiber cassumunar Roxb. attenuated type 2 inflammatory cytokine-induced tight junction disruption in airway epithelial cells.

IF 2.3 4区医学 Q3 ALLERGY

Asian Pacific journal of allergy and immunology Pub Date : 2024-11-17 DOI:10.12932/AP-180624-1873

Orapan Poachanukoon, Pasistha Termworasin, Phuntila Tharabenjasin, Thaweephol Dechatiwongse Na Ayudhya, Aekkacha Moonwiriyakit

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引用次数: 0

Abstract

Background: Barrier disruption in the airway mucosae has been implicated in allergic type 2 inflammatory diseases such as allergic rhinitis and asthma. Zingiber cassumunar Roxb. has long been used in traditional medicine to treat allergic diseases. The active compound, namely compound D, has proven anti-inflammatory benefits. However, the effect of compound D on allergic inflammation remains unclear.

Objective: This study aimed to investigate the protective effects of compound D on allergic inflammation-induced barrier disruption.

Methods: Type 2 cytokine (IL-4 and IL-13)-exposed 16HBE human bronchial epithelial cells were treated with compound D. After 24, 48, and 72 h, cytotoxicity, epithelial integrity, and tight junction (TJ) disruption were determined by viability assays, transepithelial electrical resistance measurement, and immunofluorescence staining, respectively. Moreover, the mechanism of action of compound D was investigated by western blotting.

Results: Compound D (100 and 200 µM) prevented IL-4/IL-13-induced barrier disruption at 24 and 48 h with no effect on cell viability. Compound D rescued the localization of ZO-1 to pericellular areas, and the barrier-protective effect of compound D was mediated by inhibiting STAT6 signaling.

Conclusions: Compound D can suppress IL-4/IL-13-induced epithelial inflammation and TJ disruption through STAT6 inhibition. The agent is a promising candidate for therapeutic or adjunctive treatment of type 2 inflammation-associated diseases, including asthma.

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从 Zingiber cassumunar Roxb.中提取的化合物 D 可减轻 2 型炎症细胞因子诱导的气道上皮细胞紧密连接破坏。

背景：气道粘膜屏障的破坏与过敏性鼻炎和哮喘等过敏性 2 型炎症性疾病有关。长期以来，传统医学一直使用桂枝来治疗过敏性疾病。其活性化合物，即化合物 D，已被证实具有抗炎功效。然而，化合物 D 对过敏性炎症的影响仍不清楚：本研究旨在探讨复方 D 对过敏性炎症引起的屏障破坏的保护作用：方法：用化合物D处理暴露于2型细胞因子（IL-4和IL-13）的16HBE人支气管上皮细胞，24、48和72小时后，分别通过细胞活力测定、上皮横向电阻测量和免疫荧光染色测定细胞毒性、上皮完整性和紧密连接（TJ）破坏。此外，还通过免疫印迹法研究了化合物 D 的作用机制：结果：化合物 D（100 µM和200 µM）在24小时和48小时内阻止了IL-4/IL-13诱导的屏障破坏，但对细胞活力没有影响。化合物 D 挽救了 ZO-1 在细胞周围区域的定位，化合物 D 的屏障保护作用是通过抑制 STAT6 信号传导介导的：结论：化合物 D 可通过抑制 STAT6 抑制 IL-4/IL-13 诱导的上皮炎症和 TJ 破坏。结论：化合物 D 可通过 STAT6 抑制作用抑制 IL-4/IL-13 诱导的上皮炎症和 TJ 破坏，是治疗或辅助治疗包括哮喘在内的 2 型炎症相关疾病的理想候选药物。

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

Asian Pacific journal of allergy and immunology 医学-过敏

CiteScore

12.80

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： The Asian Pacific Journal of Allergy and Immunology (APJAI) is an online open access journal with the recent impact factor (2018) 1.747 APJAI published 4 times per annum (March, June, September, December). Four issues constitute one volume. APJAI publishes original research articles of basic science, clinical science and reviews on various aspects of allergy and immunology. This journal is an official journal of and published by the Allergy, Asthma and Immunology Association, Thailand. The scopes include mechanism, pathogenesis, host-pathogen interaction, host-environment interaction, allergic diseases, immune-mediated diseases, epidemiology, diagnosis, treatment and prevention, immunotherapy, and vaccine. All papers are published in English and are refereed to international standards.