Atractylodin attenuates lipopolysaccharide-induced acute lung injury by inhibiting NLRP3 inflammasome and TLR4 pathways

被引:76
|
作者
Tang, Fayin [1 ]
Fan, Kefeng [1 ]
Wang, Kunli [1 ]
Bian, Chuanzhou [1 ]
机构
[1] Henan Univ Anim Husb & Econ, Coll Pharmaceut Engn, Longzi Hubei Rd 6, Zhengzhou, Henan 450046, Peoples R China
关键词
Atractylodin; Inflammation; Acute lung injury; NLRP3; TLR4; NF-KAPPA-B; MESENCHYMAL STEM-CELLS; SIGNALING PATHWAYS; CYTOKINES;
D O I
10.1016/j.jphs.2017.11.010
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Acute lung injury (ALI) arises from uncontrolled pulmonary inflammation with high mortality rates. Atractylodin (Atr) is a polyethylene alkynes and has been reported to possess anti-inflammation effect. Thus, we aimed to investigate the protective effect of Atr on lipopolysaccharide (LPS)-induced inflammatory responses ALI. The results indicated that Atr treatment not only significantly attenuated LPS-stimulated histopathological changes but also lessened the myeloperoxidase (MPO) activity, the wet-to-dry weight ratio of the lungs, protein leakage and infiltration of inflammatory cells. Moreover, Atr inhibited the tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-1 beta and monocyte chemoattractant protein (MCP)-1 secretion in BALF. Further study demonstrated that such inhibitory effects of Atr were due to suppression of nucleotide-binding domain-(NOD-) like receptor protein 3 (NLRP3) inflammasome and toll like receptor 4 (TLR4) activation, likely contributing to its anti-inflammatory effects. Collectively, these findings suggest that Atr may be an effective candidate for alleviating LPS-induced inflammatory responses. (C) 2018 The Authors. Production and hosting by Elsevier B.V.
引用
收藏
页码:203 / 211
页数:9
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