Oncotarget

Research Papers: Immunology:

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

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

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Oncotarget. 2016; 7:80262-80274. https://doi.org/10.18632/oncotarget.12918

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Abstract

Shuang Peng1,*, Jian Gao1,*, Wen Liu1, Chunhong Jiang2, Xiaoling Yang2, Yang Sun1, Wenjie Guo1 and Qiang Xu1

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

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

* These authors have contributed equally to this work

Correspondence to:

Qiang Xu, email:

Wenjie Guo, email:

Yang Sun, email:

Keywords: andrographolide; asthma; NF-κB; NLRP3; ROS; Immunology and Microbiology Section; Immune response; Immunity

Received: August 15, 2016 Accepted: October 14, 2016 Published: October 26, 2016

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.


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