, Volume 39, Issue 1, pp 327–335 | Cite as

Etomidate Mitigates Lipopolysaccharide-Induced CD14 and TREM-1 Expression, NF-κB Activation, and Pro-inflammatory Cytokine Production in Rat Macrophages

  • Ming Liu
  • Yu Zhang
  • Jun-Yu Xiong
  • Yan Wang
  • Shen Lv


This study was aimed at investigating the effect of etomidate on the viability of rat macrophages and the function of lipopolysaccharide (LPS)-stimulated macrophages as well as the potential mechanisms. Rat macrophages were isolated and treated with different doses of etomidate for 24 h, and their viability was determined by the CCK-8 assay. Furthermore, macrophages were treated with, or without, 1 μg/ml of LPS, and/or 2.5 or 5 μM etomidate in the presence or absence of a TREM-1 inhibitor (LP17, 100 ng/ml), and the levels of TNF-α, IL-6, CD14, and TREM-1 in the different groups of cells were determined by quantitative RT-PCR, ELISA, and Western blot assays. The levels of NF-κB activation in the different groups of cells were analyzed by an electrophoretic mobility shift assay (EMSA). Etomidate at 31.25 μM or a low dose did not affect the viability of rat macrophages, while etomidate at higher doses reduced the viability of macrophages in vitro. Treatment with 2.5 or 5 μM etomidate or with LP17 alone did not affect the levels of TNF-α, IL-6, CD-14, and TREM-1 in macrophages. Treatment with etomidate significantly mitigated LPS-stimulated TNF-α, IL-6, CD-14, and TREM-1 expression (p < 0.05 for all) and inhibited LPS-induced NF-κB activation in macrophages in vitro. However, treatment with both etomidate and LP17 did not enhance the inhibitory effects in macrophages. Hence, etomidate mitigates LPS-up-regulated pro-inflammatory cytokine production and inhibits LPS-enhanced CD14 and TREM-1 expression and NF-κB activation in macrophages.


etomidate macrophages sepsis lipopolysaccharide inflammation NF-κB 



This work was supported by a grant from the National Natural Science Foundation of China (no. 81171791).

Conflict of Interest

The authors declare no conflicts of interest.


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Copyright information

© Springer Science+Business Media New York 2015

Authors and Affiliations

  • Ming Liu
    • 1
  • Yu Zhang
    • 1
  • Jun-Yu Xiong
    • 1
  • Yan Wang
    • 2
  • Shen Lv
    • 2
  1. 1.Department of AnesthesiologyThe Second Hospital of Dalian Medical UniversityDalianChina
  2. 2.Laboratory of Molecular Biologythe Second Hospital of Dalian Medical UniversityDalianChina

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