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18-甘草次酸对真菌蛋白酶诱导的气道炎症反应的影响。

Effects of 18-Glycyrrhetinic Acid on Fungal Protease-Induced Airway Inflammatory Responses.

机构信息

Graduate School of Medical Science and Engineering, Biomedical Research Center, KAIST Institute for the BioCentury, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea.

Korean Medicine Convergence Research Division, Korea Institute of Oriental Medicine (KIOM), Daejeon 34054, Republic of Korea.

出版信息

Mediators Inflamm. 2018 May 15;2018:6461032. doi: 10.1155/2018/6461032. eCollection 2018.

DOI:10.1155/2018/6461032
PMID:29861658
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5976916/
Abstract

Airway epithelial cells secrete diverse inflammatory mediators in response to various stimuli. Thus, early regulation of immune responses in the airway epithelium is likely critical for the control of chronic inflammatory diseases. The purpose of the present study was to evaluate the effects of 18-glycyrrhetinic acid (GA) on inflammatory responses generated in response to a fungal protease allergen that induces epithelial damage. To understand the underlying mechanisms, we also investigated the inhibitory effects of GA on the production of mitochondrial reactive oxygen species (ROS) in the human bronchial epithelial cell line BEAS2B. In this study, GA treatment reduced cytokine production and the human neutrophil cell line HL60 migration through decreased mitochondrial ROS production. In addition, GA significantly reduced inflammatory cell infiltration and cytokine levels in the bronchoalveolar lavage (BAL) fluid of fungal allergen-administered mice. Inhibitory effects of GA are dependent on the mitochondrial ROS/MAPK axis. Moreover, the effect of GA on the regulation of mitochondrial ROS depends on the expression of uncoupling protein-2 (UCP-2). Taken together, GA might represent a potential therapeutic agent for blocking inflammatory responses in airways.

摘要

气道上皮细胞在受到各种刺激时会分泌多种炎症介质。因此,早期调节气道上皮的免疫反应可能对控制慢性炎症性疾病至关重要。本研究旨在评估 18-甘草次酸 (GA) 对诱导上皮损伤的真菌蛋白酶变应原引起的炎症反应的影响。为了了解潜在的机制,我们还研究了 GA 对人支气管上皮细胞系 BEAS2B 中线粒体活性氧 (ROS) 产生的抑制作用。在这项研究中,GA 处理通过减少线粒体 ROS 的产生,减少细胞因子的产生和人中性粒细胞 HL60 的迁移。此外,GA 还显著减少了真菌变应原给药小鼠支气管肺泡灌洗液 (BAL) 中的炎症细胞浸润和细胞因子水平。GA 的抑制作用依赖于线粒体 ROS/MAPK 轴。此外,GA 对线粒体 ROS 调节的作用取决于解偶联蛋白-2 (UCP-2) 的表达。总之,GA 可能代表一种潜在的治疗剂,可阻断气道中的炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/81eb78a08a67/MI2018-6461032.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/6976edacbacd/MI2018-6461032.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/1e1b59f0a182/MI2018-6461032.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/6e1aed76d965/MI2018-6461032.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/3b9aea95f785/MI2018-6461032.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/81eb78a08a67/MI2018-6461032.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/6976edacbacd/MI2018-6461032.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/ed28e7631305/MI2018-6461032.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/3aac532950b1/MI2018-6461032.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/1e1b59f0a182/MI2018-6461032.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/6e1aed76d965/MI2018-6461032.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/3b9aea95f785/MI2018-6461032.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f3a/5976916/81eb78a08a67/MI2018-6461032.007.jpg

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