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

// Shuang Peng 1,* , Jian Gao 1,* , Wen Liu 1 , Chunhong Jiang 2 , Xiaoling Yang 2 , Yang Sun 1 , Wenjie Guo 1 and Qiang Xu 1 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.