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穿心莲内酯通过抑制活性氧介导的核因子κB信号通路和NLRP3炎性小体激活来改善卵清蛋白诱导的小鼠肺损伤。

Andrographolide ameliorates OVA-induced lung injury in mice by suppressing ROS-mediated NF-κB signaling and NLRP3 inflammasome activation.

作者信息

Peng Shuang, Gao Jian, Liu Wen, Jiang Chunhong, Yang Xiaoling, Sun Yang, Guo Wenjie, Xu Qiang

机构信息

State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.

State Key Laboratory of Innovative Nature Medicine and TCM Injections, Jiangxi Qingfeng Pharmaceutical Co., Ltd., Ganzhou, China.

出版信息

Oncotarget. 2016 Dec 6;7(49):80262-80274. doi: 10.18632/oncotarget.12918.

DOI:10.18632/oncotarget.12918
PMID:27793052
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5348318/
Abstract

In this study, we attempted to explore the effect and possible mechanism of Andrographolide on OVA-induced asthma. OVA challenge induced significant airway inflammatory cell recruitment and lung histological alterations, which were ameliorated by Andrographolide. The protein levels of cytokines in bron-choalveolar fluid (BALF) and serum were reduced by Andrographolide administration as well as the mRNA levels in lung tissue. Mechanically, Andrographolide markedly hampered the activation of nuclear factor-κB (NF-κB) and NLRP3 inflammasome both in vivo and vitro thus decreased levels of TNF-α and IL-1β. Finally, we confirmed that ROS scavenging was responsible for Andrographolide's inactivation of NF-κB and NLRP3 inflammasome signaling. Our study here revealed the effect and possible mechanism of Andrographolide on asthma, which may represent a new therapeutic approach for treating this disease.

摘要

在本研究中,我们试图探讨穿心莲内酯对卵清蛋白(OVA)诱导的哮喘的作用及可能机制。OVA激发诱导了显著的气道炎症细胞募集和肺部组织学改变,而穿心莲内酯可改善这些改变。给予穿心莲内酯后,支气管肺泡灌洗液(BALF)和血清中细胞因子的蛋白质水平以及肺组织中的mRNA水平均降低。从机制上讲,穿心莲内酯在体内和体外均显著抑制核因子-κB(NF-κB)和NLRP3炎性小体的激活,从而降低肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)的水平。最后,我们证实活性氧清除是穿心莲内酯使NF-κB和NLRP3炎性小体信号失活的原因。我们在此的研究揭示了穿心莲内酯对哮喘的作用及可能机制,这可能代表了一种治疗该疾病的新方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/6fec6c4a90a5/oncotarget-07-80262-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/95699c4922fe/oncotarget-07-80262-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/f4d111e81e36/oncotarget-07-80262-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/41ff55dd7d31/oncotarget-07-80262-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/0a716df13cca/oncotarget-07-80262-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/3d3136ca2bb0/oncotarget-07-80262-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/213dedbcf4fc/oncotarget-07-80262-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/3642ada905f0/oncotarget-07-80262-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/0dcc3936eea5/oncotarget-07-80262-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/876701656870/oncotarget-07-80262-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/6fec6c4a90a5/oncotarget-07-80262-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/95699c4922fe/oncotarget-07-80262-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/f4d111e81e36/oncotarget-07-80262-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/41ff55dd7d31/oncotarget-07-80262-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/0a716df13cca/oncotarget-07-80262-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/3d3136ca2bb0/oncotarget-07-80262-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/213dedbcf4fc/oncotarget-07-80262-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/3642ada905f0/oncotarget-07-80262-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/0dcc3936eea5/oncotarget-07-80262-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/876701656870/oncotarget-07-80262-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e65/5348318/6fec6c4a90a5/oncotarget-07-80262-g010.jpg

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