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Inflammation Research

, Volume 56, Issue 8, pp 324–333 | Cite as

Effects of lipoxin A4 on lipopolysaccharide induced proliferation and reactive oxygen species production in RAW264.7 macrophages through modulation of G-CSF secretion

  • X.-Y. Zhou
  • P. Wu
  • L. Zhang
  • W. Xiong
  • Y.-S. Li
  • Y.-M. Feng
  • D.-Y. Ye
Article

Abstract:

Objective:

To investigate the effects of lipoxin A4 (LXA4) on lipopolysaccharide (LPS) induced proliferation and reactive oxygen species production in RAW264.7 macrophages.

Methods:

RAW264.7 macrophages were treated with or without LPS in the absence or presence of LXA4. In another experiment, the cells were incubated with rmG-CSF (recombinant mouse granulocyte-colony stimulating factor) or neutralizing anti-G-CSF Ab in the absence or presence of LPS and LXA4. The proliferation effects were detected by Cell Counting Kit-8 assay. Reative oxygen species were quantified by flow cytometry and laser confocal scanning microscopy. G-CSF gene expression and protein secretion were measured by real time PCR and ELISA, respectively. IκBα degradation and NF-κB translocation were determined by Western blot, and NF-κB transcriptional activity was tested by transfections and luciferase activities assay.

Results:

(1) LXA4 controlled LPS-induced proliferation and reactive oxygen species production. (2) LXA4 decreased LPS-induced G-CSF gene expression and protein secretion. (3) LXA4 restrained LPS-induced IκBα degradation, NF-κB translocation, and NF-κB transcriptional activity. (4) rmG-CSF could rescue the inhibitory effects of LXA4, and neutralizing anti-G-CSF Ab was able to enhance the roles of LXA4.

Conclusions:

LXA4 inhibited LPS-induced proliferation and reactive oxygen species production in RAW264.7 macrophages partially through modulation of G-CSF secretion.

Keywords:

Macrophages Lipopolysaccharide Eicosanoids Inflammatory mediator Inflammation 

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Copyright information

© Birkhäuser Verlag, Basel 2007

Authors and Affiliations

  • X.-Y. Zhou
    • 1
  • P. Wu
    • 1
  • L. Zhang
    • 1
  • W. Xiong
    • 1
  • Y.-S. Li
    • 1
  • Y.-M. Feng
    • 2
  • D.-Y. Ye
    • 1
  1. 1.Department of Pathophysiology, Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanP. R. China
  2. 2.Department of Biochemistry and Molecular Biolog, Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina

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