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

  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},
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… 

C/EBPγ is a critical negative regulator of LPS‐/IgG immune complex‐induced acute lung injury through the downregulation of C/EBPβ‐/C/EBPδ‐dependent C/EBP transcription activation

It is found that adenovirus‐mediated C/EBPγ expression in the lung tissue alleviates LPS‐/IgG immune complexes‐stimulated acute pulmonary damage through reducing vascular permeability changes and recruitment of neutrophils into alveolar spaces, which might be linked to a decrease in the production of pro‐inflammatory mediators, such as TNF‐α and IL‐6.

H2S attenuates acute lung inflammation induced by administration of lipopolysaccharide in adult male rats.

It is proved that H2S has a protective effect against LPS induced ALI due to its anti-nitrative, anti-oxidant and anti-inflammatory properties.

Expression level of 12-amino acid triggering receptor on myeloid cells-like transcript 1 derived peptide alleviates lipopolysaccharide-induced acute lung injury in mice.

LPS‑induced pathohistological injury, edema and neutrophil infiltration were significantly alleviated by TREM‑1 inhibitor, LR12, and the proinflammatory cytokines and chemokines were significantly reduced, whereas the anti‑inflammatory cytokine, IL‑10 were significantly increased by LR12.

Induction of apoptosis by Bigelovii A through inhibition of NF-κB activity

Bigelovii A significantly inhibited the proliferation of human breast cancer cells in a concentration-dependent manner and downregulated the constitutive activation of nuclear factor (NF)-κB, as indicated by the electrophoretic mobility gel shift assay and immunocytochemistry.



Genistein prevents nuclear factor-kappa B activation and acute lung injury induced by lipopolysaccharide.

  • J. KangH. Lee Y. Koh
  • Biology, Medicine
    American journal of respiratory and critical care medicine
  • 2001
Results suggest that genistein attenuates LPS-induced acute lung responses through inhibition of NF-kappaB activation, which appears to be an important mechanism mediating L PS-induced CINC production and MMP-9 activity and resulting neutrophil recruitment associated with acute lung inflammation and injury.

Myeloid depletion of SOCS3 enhances LPS‐induced acute lung injury through CCAAT/enhancer binding protein δ pathway

Results indicate that SOCS3 has a protective role in LPS‐induced ALI by suppressing C/EBPδ activity in the lung through CCAAT/enhancer binding protein δ pathway.

C5a-regulated CCAAT/Enhancer-binding Proteins β and δ Are Essential in Fcγ Receptor-mediated Inflammatory Cytokine and Chemokine Production in Macrophages*

The data suggest that C/EBPβ and -δ are key regulators for FcγR-mediated induction of cytokines and chemokines in macrophages, and the evidence that C5a regulates IgG IC-induced inflammatory responses by enhancing ERK1/2 and p38 MAPK activities as well as C-δ activities is provided.

Essential Role of Alveolar Macrophages in Intrapulmonary Activation of NF- κ B

In the present studies, rat lungs were depleted of alveolar macrophages by airway instillation of liposome-encapsulated dichloromethylene diphosphonate, and bronchoalveolar lavage levels of tumor necrosis factor-α and the CXC chemokine, macrophage inflammatory protein-2, were substantially reduced.

Macrophages Are Necessary for Maximal Nuclear Factor- κ B Activation in Response to Endotoxin

Combined IT + IV clodronate treatment markedly reduced lung NF- κ B activation and the intensity of neutrophilic alveolitis after intrape...

Differential NF-κB activation after intratracheal endotoxin.

IT LPS causes differential NF-κB activation in air space cells and lung tissue, which likely determines production of key cytokines and directs the evolution of neutrophilic alveolitis.

Characterization of a Murine Model of Endotoxin-Induced Acute Lung Injury

The characterization of this murine model of endotoxin-induced microvascular injury in mice will facilitate its utilization in ARDS research.

Alveolar macrophage activation is a key initiation signal for acute lung ischemia-reperfusion injury.

It is concluded that alveolar macrophages are an essential player in the initiation of acute lung I/R injury and are a major producer/initiator of TNF-alpha, MCP-1, and MIP-2.

Protective Actions of Aspirin-Triggered (17R) Resolvin D1 and Its Analogue, 17R-Hydroxy-19-Para-Fluorophenoxy-Resolvin D1 Methyl Ester, in C5a-Dependent IgG Immune Complex–Induced Inflammation and Lung Injury

It is demonstrated that IgG immune complex–induced activation of NF-κB and C/EBPβ transcription factors in the lung was significantly inhibited by AT-RVD1 and p-RvD1, and a new approach to the blocking of immune complex-induced inflammation is suggested.