Post-Intake of S-Ethyl Cysteine and S-Methyl Cysteine Improved LPS-Induced Acute Lung Injury in Mice
- PMID: 27548215
- PMCID: PMC4997420
- DOI: 10.3390/nu8080507
Post-Intake of S-Ethyl Cysteine and S-Methyl Cysteine Improved LPS-Induced Acute Lung Injury in Mice
Retraction in
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Retraction: Hsia et al. Post-Intake of S-Ethyl Cysteine and S-Methyl Cysteine Improved LPS-Induced Acute Lung Injury in Mice. Nutrients 2016, 8, 507.Nutrients. 2017 May 23;9(6):528. doi: 10.3390/nu9060528. Nutrients. 2017. PMID: 28545223 Free PMC article.
Abstract
The effects of S-ethyl cysteine (SEC) and S-methyl cysteine (SMC) on lipopolysaccharide (LPS)-induced acute lung injury in mice were examined. Eight hours after LPS challenge, SEC or SMC was supplied in drinking water at 0.5% or 1% for 3 days. LPS increased lung myeloperoxidase activity, neutrophil counts and edema. SEC or SMC post-intake attenuated these events. SEC or SMC suppressed LPS-induced lung expression of cyclooxygenase-2, nuclear factor-κB and mitogen-activated protein kinase, and lowered the generation of tumor necrosis factor-alpha, monocyte chemoattractant protein-1 and prostaglandin E₂. LPS enhanced the expression of p47(phox), gp91(phox), Bax and cleaved caspase-3, and increased the production of reactive oxygen species in the lung. SEC or SMC post-intake reversed these alterations. These findings suggest that these agents could protect the lung through their anti-inflammatory, anti-oxidative and anti-apoptotic activities.
Keywords: LPS; S-ethyl cysteine; S-methyl cysteine; inflammation; lung.
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