Road Closures Near 801 Broadway Parking Garage
News & Updates
Search Research Content
Resource Finder at Kennedy Krieger Institute
A free resource that provides access to information and support for individuals and families living with developmental disabilities.
Unfractionated Heparin Ameliorates Lipopolysaccharide-Induced Lung Inflammation by Downregulating Nuclear Factor-κB Signaling Pathway.
|Title||Unfractionated Heparin Ameliorates Lipopolysaccharide-Induced Lung Inflammation by Downregulating Nuclear Factor-κB Signaling Pathway.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Li X, Li Z, Zheng Z, Liu Y, Ma X|
|Date Published||2013 Dec|
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.