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

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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.

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Acknowledgments

The authors give special thanks to Dr. Liang Wang (Department of Pathology, China Medical University) for the pathological analysis. The research which discussed unfractionated heparin was supported by the National Natural Science Foundation of China (81101411).

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The author declares that there are no conflicts of interest.

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Correspondence to Xiaochun Ma.

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Li, X., Li, Z., Zheng, Z. et al. Unfractionated Heparin Ameliorates Lipopolysaccharide-Induced Lung Inflammation by Downregulating Nuclear Factor-κB Signaling Pathway. Inflammation 36, 1201–1208 (2013). https://doi.org/10.1007/s10753-013-9656-5

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