β-Nicotinamide adenine dinucleotide attenuates lipopolysaccharide-induced inflammatory effects in a murine model of acute lung injury.

Experimental Lung Research
Nagavedi S UmapathyAlexander D Verin

Abstract

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) occur in approximately 200,000 patients per year. Studies indicate that lung endothelium plays a significant role in ALI. The authors' recent in vitro studies demonstrate a novel mechanism of β-nicotinamide adenine dinucleotide (β-NAD)-induced protection against gram-positive (pneumolysin, PLY) and gram-negative (lipopolysaccharide, LPS) toxin-induced lung endothelial cell (EC) barrier dysfunction. The objective of the current study was to evaluate the protective effect of β-NAD against LPS-induced ALI in mice. C57BL/6J mice were randomly divided into 4 groups: vehicle, β-NAD, LPS, and LPS/β-NAD. After surgery, mice were allowed to recover for 24 hours. Evans blue dye-albumin (EBA) was given through the internal jugular vein 2 hours prior to the termination of the experiments. Upon sacrificing the animals, bronchoalveolar lavage fluid (BALF) was collected and the lungs were harvested. β-NAD treatment significantly attenuated the inflammatory response by means of reducing the accumulation of cells and protein in BALF, blunting the parenchymal neutrophil infiltration, and preventing capillary leak. In addition, the histological examination demonstrated decreas...Continue Reading

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Feb 8, 2014·PloS One·Feng ChenDavid J R Fulton
Oct 8, 2014·Nature Communications·Stefan G TulliusAbdallah ElKhal
Jan 15, 2014·American Journal of Physiology. Lung Cellular and Molecular Physiology·Joyce N GonzalesAlexander D Verin
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Dec 7, 2017·Journal of Cellular and Molecular Medicine·Harshavardhan JangaSabine Fuchs
Apr 13, 2018·International Journal of Molecular Sciences·Sebastian Daniel HillerVeronika Grau

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