Inflammation

, Volume 36, Issue 6, pp 1201–1208

Unfractionated Heparin Ameliorates Lipopolysaccharide-Induced Lung Inflammation by Downregulating Nuclear Factor-κB Signaling Pathway

  • Xu Li
  • ZhiLiang Li
  • Zhen Zheng
  • Yina Liu
  • Xiaochun Ma
Article

DOI: 10.1007/s10753-013-9656-5

Cite this article as:
Li, X., Li, Z., Zheng, Z. et al. Inflammation (2013) 36: 1201. doi:10.1007/s10753-013-9656-5

Abstract

The present study aimed to determine the protective effects and the underlying mechanisms of unfractionated heparin on lipopolysaccharide (LPS)-induced endotoxemia and lung injury in rats. Rats were injected intravenously with LPS at 6 mg/kg. We examined the therapeutic effects of unfractionated heparin (100 or 300 U/kg) on LPS-induced endotoxemia by dosing intravenously simultaneously after LPS challenge. The animal lung edema degree was evaluated by wet/dry weight ratio. The levels of inflammatory mediators including interleukin-1β (IL-1β) and interleukin-6 (IL-6) were assayed by enzyme-linked immunosorbent assay and quantitative real-time RT-PCR. The activation of nuclear factor-κB (NF-κB) was evaluated by Western blotting. The investigations revealed that treatment with unfractionated heparin can attenuate inflammatory responses in a rat model of LPS-induced acute lung injury, and the effect was much better in 300 U/kg group. The mechanisms by which unfractionated heparin exerts its anti-inflammatory effect are correlated with inhibition of IL-1β and IL-6 production via inactivation of NF-κB.

KEY WORDS

unfractionated heparinlipopolysaccharideendotoxemiaacute lung injurynuclear factor-κB

Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  • Xu Li
    • 1
  • ZhiLiang Li
    • 1
  • Zhen Zheng
    • 1
  • Yina Liu
    • 1
  • Xiaochun Ma
    • 1
  1. 1.Department of Intensive Care Unitthe First Affiliated Hospital, China Medical UniversityShenyangPeople’s Republic of China