Sodium butyrate alleviates LPS-induced acute lung injury in mice via inhibiting HMGB1 release

Sodium butyrate alleviates LPS-induced acute lung injury in mice via inhibiting HMGB1 release Sodium butyrate (SB) is a short chain 4-carbon fatty acid salt naturally exists in animal fats. Previous studies have proven that sodium butyrate has many beneficial functions such as anti-tumor and anti-inflammatory actions. In the current study we investigated the effect and possible mechanism of sodium butyrate in LPS-induced acute lung injury (ALI). ALI was induced by intratracheal administration of LPS (10 mg/kg) in male BALB/c mice. Sodium butyrate (500 mg/kg) was administered intraperitoneally 30 min prior to LPS exposure. We found that sodium butyrate significantly protected animals from LPS-induced ALI as evidenced by decreased the lung wet to dry weight ratio, total cells, neutrophils, macrophages, myeloperoxidase (MPO) activity, and lung histological damage compared to vehicle control. Sodium butyrate pretreatment markedly inhibited the production of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Furthermore, sodium butyrate pretreatment dramatically suppressed HMGB1 release and NF-κ B activation. Together, these results suggest that sodium butyrate pretreatment protects mice from LPS-induced acute lung injury, possibly through the modulation of HMGB1 and inflammatory responses. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png International Immunopharmacology Elsevier

Sodium butyrate alleviates LPS-induced acute lung injury in mice via inhibiting HMGB1 release

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Publisher
Elsevier
Copyright
Copyright © 2018 Elsevier Ltd
ISSN
1567-5769
eISSN
1878-1705
D.O.I.
10.1016/j.intimp.2018.01.017
Publisher site
See Article on Publisher Site

Abstract

Sodium butyrate (SB) is a short chain 4-carbon fatty acid salt naturally exists in animal fats. Previous studies have proven that sodium butyrate has many beneficial functions such as anti-tumor and anti-inflammatory actions. In the current study we investigated the effect and possible mechanism of sodium butyrate in LPS-induced acute lung injury (ALI). ALI was induced by intratracheal administration of LPS (10 mg/kg) in male BALB/c mice. Sodium butyrate (500 mg/kg) was administered intraperitoneally 30 min prior to LPS exposure. We found that sodium butyrate significantly protected animals from LPS-induced ALI as evidenced by decreased the lung wet to dry weight ratio, total cells, neutrophils, macrophages, myeloperoxidase (MPO) activity, and lung histological damage compared to vehicle control. Sodium butyrate pretreatment markedly inhibited the production of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Furthermore, sodium butyrate pretreatment dramatically suppressed HMGB1 release and NF-κ B activation. Together, these results suggest that sodium butyrate pretreatment protects mice from LPS-induced acute lung injury, possibly through the modulation of HMGB1 and inflammatory responses.

Journal

International ImmunopharmacologyElsevier

Published: Mar 1, 2018

References

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