s‐Ethyl Cysteine and s‐Methyl Cysteine Protect Human Bronchial Epithelial Cells Against Hydrogen Peroxide Induced Injury

Protective effects and actions from s‐ethyl cysteine (SEC) and s‐methyl cysteine (SMC) for BEAS‐2B cells were examined. BEAS‐2B cells were pretreated with SEC or SMC at 4, 8, or 16 μmol/L, and followed by hydrogen peroxide (H₂O₂) treatment. Data showed that H₂O₂ enhanced Bax, caspase‐3 and caspase‐8 expression, and declined Bcl‐2 expression. However, SEC or SMC dose‐dependently decreased caspase‐3 expression and reserved Bcl‐2 expression. H₂O₂ increased reactive oxygen species (ROS) production, and lowered glutathione level, glutathione peroxide, and glutathione reductase activities in BEAS‐2B cells. SEC or SMC pretreatments reduced ROS generation, and maintained glutathione redox cycle in those cells. H₂O₂ upregulated the expression of both p47^phox and gp91^phox. SEC and SMC downregulated p47^phox expression. SEC or SMC at 8 and 16 μmol/L decreased H₂O₂‐induced release of inflammatory cytokines. H₂O₂ stimulated the activation of nuclear factor‐κB (NF‐κB) and mitogen‐activated protein kinase. SEC and SMC pretreatments dose‐dependently downregulated NF‐κB p65 and p‐p38 expression. Pyrrolidine dithiocarbamate or SB203580 inhibited NF‐κB activation and p38 phosphorylation; thus, SEC or SMC pretreatments failed to affect protein expression of these factors. These novel findings suggest that SEC or SMC could protect bronchial cells and benefit respiratory epithelia stability and functions.