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水提取物对人中性粒细胞具有抗炎作用,并可减轻咪喹莫特诱导的小鼠银屑病样皮肤炎症。

Water Extract Exhibits Anti-inflammatory Effects in Human Neutrophils and Alleviates Imiquimod-Induced Psoriasis-Like Skin Inflammation in Mice.

作者信息

Cheng Wei-Jen, Chiang Chih-Chao, Lin Cheng-Yu, Chen Yu-Li, Leu Yann-Lii, Sie Jia-Yu, Chen Wen-Ling, Hsu Chung-Yuan, Kuo Jong-Jen, Hwang Tsong-Long

机构信息

Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan.

School of Traditional Chinese Medicine, College of Medicine, Chang Gung University, Taoyuan, Taiwan.

出版信息

Front Pharmacol. 2021 Dec 10;12:762829. doi: 10.3389/fphar.2021.762829. eCollection 2021.

DOI:10.3389/fphar.2021.762829
PMID:34955833
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8707293/
Abstract

Neutrophils are the primary immune cells in innate immunity, which are related to various inflammatory diseases. is a Chinese medicinal herb used to treat various oxidative stress-related inflammatory diseases. However, there are limited studies that elucidate the effects of in human neutrophils. In this study, we used isolated human neutrophils activated by various stimulants to investigate the anti-inflammatory effects of water extract (AWE). Cell-free assays were used to examine free radicals scavenging capabilities on superoxide anion, reactive oxygen species (ROS), and nitrogen-centered radicals. Imiquimod (IMQ) induced psoriasis-like skin inflammation mouse model was used for investigating anti-psoriatic effects. We found that AWE inhibited superoxide anion production, ROS generation, and elastase release in human neutrophils, which exhibiting a direct anti-neutrophil effect. Moreover, AWE exerted a ROS scavenging ability in the 2,2'-Azobis (2-amidinopropane) dihydrochloride assay, but not superoxide anion in the xanthine/xanthine oxidase assay, suggesting that AWE exhibited anti-oxidation and anti-inflammatory capabilities by both scavenging ROS and by directly inhibiting neutrophil activation. AWE also reduced CD11b expression and adhesion to endothelial cells in activated human neutrophils. Meanwhile, in mice with psoriasis-like skin inflammation, administration of topical AWE reduced both the affected area and the severity index score. It inhibited neutrophil infiltration, myeloperoxidase release, ROS-induced damage, and skin proliferation. In summary, AWE exhibited direct anti-inflammatory effects by inhibiting neutrophil activation and anti-psoriatic effects in mice with IMQ-induced psoriasis-like skin inflammation. Therefore, AWE could potentially be a pharmaceutical Chinese herbal medicine to inhibit neutrophilic inflammation for anti-psoriasis.

摘要

中性粒细胞是固有免疫中的主要免疫细胞,与多种炎症性疾病相关。[此处原文缺失一种中药材名称]是一种用于治疗各种氧化应激相关炎症性疾病的中药材。然而,阐明[该中药材名称]对人中性粒细胞作用的研究有限。在本研究中,我们使用分离的、由各种刺激剂激活的人中性粒细胞来研究[该中药材名称]水提取物(AWE)的抗炎作用。采用无细胞试验检测其对超氧阴离子、活性氧(ROS)和氮中心自由基的自由基清除能力。使用咪喹莫特(IMQ)诱导的银屑病样皮肤炎症小鼠模型来研究其抗银屑病作用。我们发现AWE抑制人中性粒细胞中超氧阴离子的产生、ROS的生成和弹性蛋白酶的释放,表现出直接的抗中性粒细胞作用。此外,AWE在2,2'-偶氮二异丁脒二盐酸盐试验中具有ROS清除能力,但在黄嘌呤/黄嘌呤氧化酶试验中对超氧阴离子无清除能力,这表明AWE通过清除ROS和直接抑制中性粒细胞激活展现出抗氧化和抗炎能力。AWE还降低了活化的人中性粒细胞中CD11b的表达以及与内皮细胞的黏附。同时,在患有银屑病样皮肤炎症的小鼠中,局部给予AWE可减少病变面积和严重程度指数评分。它抑制中性粒细胞浸润、髓过氧化物酶释放、ROS诱导的损伤和皮肤增殖。总之,AWE通过抑制中性粒细胞激活表现出直接的抗炎作用,并对IMQ诱导的银屑病样皮肤炎症小鼠具有抗银屑病作用。因此,AWE有可能成为一种抑制中性粒细胞炎症以治疗银屑病的药用中药材。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/d754a0adefea/fphar-12-762829-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/d0ac76290528/fphar-12-762829-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/7ae39a6bd5ff/fphar-12-762829-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/edf57b8bafbb/fphar-12-762829-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/3057741e38f1/fphar-12-762829-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/e9b700bb27d8/fphar-12-762829-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/c125d295a45c/fphar-12-762829-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/0bb8abcdd2b8/fphar-12-762829-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/d564867d449d/fphar-12-762829-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/d754a0adefea/fphar-12-762829-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/d0ac76290528/fphar-12-762829-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/7ae39a6bd5ff/fphar-12-762829-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/edf57b8bafbb/fphar-12-762829-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/3057741e38f1/fphar-12-762829-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/e9b700bb27d8/fphar-12-762829-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/c125d295a45c/fphar-12-762829-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/0bb8abcdd2b8/fphar-12-762829-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/d564867d449d/fphar-12-762829-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dd7/8707293/d754a0adefea/fphar-12-762829-g009.jpg

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