• DOI:10.1155/2016/9201604
• Corpus ID: 31112625

Bigelovii A Protects against Lipopolysaccharide-Induced Acute Lung Injury by Blocking NF-κB and CCAAT/Enhancer-Binding Protein δ Pathways

@article{Yan2016BigeloviiAP,
  title={Bigelovii A Protects against Lipopolysaccharide-Induced Acute Lung Injury by Blocking NF-$\kappa$B and CCAAT/Enhancer-Binding Protein $\delta$ Pathways},
  author={Chunguang Yan and Fuqin Guan and Yanfei Shen and Huifang Tang and Dong Yuan and Hongwei Gao and Xujun Feng},
  journal={Mediators of Inflammation},
  year={2016},
  volume={2016}
}

• Chunguang Yan, Fuqin Guan, +4 authors Xujun Feng
• Published 19 April 2016
• Biology, Chemistry, Medicine
• Mediators of Inflammation

Optimal methods are applied to acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS), but the mortality rate is still high. Accordingly, further studies dedicated to identify novel therapeutic approaches to ALI are urgently needed. Bigelovii A is a new natural product and may exhibit anti-inflammatory activity. Therefore, we sought to investigate its effect on lipopolysaccharide- (LPS-) induced ALI and the underlying mechanisms. We found that LPS-induced ALI was significantly alleviated by Bigelovii A treatment, characterized by reduction of proinflammatory mediator production, neutrophil infiltration, and lung permeability. Furthermore, Bigelovii A also downregulated LPS-stimulated inflammatory mediator expressions in vitro. Moreover, both NF-κB and CCAAT/enhancer-binding protein δ (C/EBPδ) activation were obviously attenuated by Bigelovii A treatment. Additionally, phosphorylation of both p38 MAPK and ERK1/2 (upstream signals of C/EBPδ activation) in response to LPS challenge was also inhibited by Bigelovii A. Therefore, Bigelovii A could attenuate LPS-induced inflammation by suppression of NF-κB, inflammatory mediators, and p38 MAPK/ERK1/2—C/EBPδ, inflammatory mediators signaling pathways, which provide a novel theoretical basis for the possible application of Bigelovii A in clinic.