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 p47phox, gp91phox, 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.
Highlights
Acute lung injury (ALI), a complicated respiratory disorder with a high morbidity rate, is characterized by pulmonary edema, inflammation, alveolar barrier disruption, capillary leak and hypoxemia [1,2]
It is reported that nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways play crucial roles in the inflammatory progression of ALI, and the activation of these pathways promotes the excessive release of cytokines and chemokines including interleukin (IL)-6, tumor necrosis factor (TNF)-alpha and monocyte chemoattractant protein (MCP)-1 [3,4]
The detected bands were processed by an image analyzer, and the blot was quantified and normalized against glyceraldehyde-3-phosphate dehydrogenase (GAPDH), which was used for loading control
Summary
Acute lung injury (ALI), a complicated respiratory disorder with a high morbidity rate, is characterized by pulmonary edema, inflammation, alveolar barrier disruption, capillary leak and hypoxemia [1,2]. Our other study indicated that SEC or SMC ameliorated H2 O2 -induced apoptotic, oxidative and inflammatory injury in human BEAS-2B cells (bronchial cells) through preserving Bcl-2 expression, decreasing ROS formation and limiting protein expression of NAPDH oxidase, NF-κB and MAPK [16]. Those previous studies suggest that SEC and SMC are agents with anti-oxidative and anti-inflammatory activities, and may be able to protect the lung. The impact of these agents upon protein expression of COX-2, NF-κB, MAPK, NADPH oxidase and Bcl-2 in the lung was evaluated
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