Abstract
The aim of this study was to investigate the effect and mechanism of action of chloral hydrate on the peptidoglycan (PGN)-induced inflammatory macrophage response. The effect of chloral hydrate on the production of tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) by murine peritoneal macrophages with PGN-stimulation was investigated. In addition, RAW264.7 cells transfected with a nuclear factor-κB (NF-κB) luciferase reporter plasmid stimulated by PGN were used to study the effect of chloral hydrate on the levels NF-κB activity. Flow cytometry and western blotting were performed to investigate the expression levels of toll-like receptor 2 (TLR2) in the treated RAW264.7 cells. It was identified that chloral hydrate reduced the levels of IL-6 and TNF-α produced by the peritoneal macrophages stimulated with PGN. The levels of NF-κB activity of the RAW264.7 cells stimulated by PGN decreased following treatment with chloral hydrate, which was associated with a reduction in the expression levels of TLR2 and reduced levels of TLR2 signal transduction. These data demonstrate that chloral hydrate reduced the magnitude of the PGN-induced inflammatory macrophage response associated with lower expression levels of TLR2.
Highlights
Chloral hydrate is a well‐known sedative and anesthetic that is used in pediatric procedures, including echocardiograms and magnetic resonance imaging [1,2,3,4,5], and in animal experiments [6,7,8,9]
It was demonstrated that therapeutic concentrations of chloral hydrate delayed and reduced the magnitude of the inflammatory response and improved the survival rate of mice following the induction of liver injury with lipopolysaccharide and D‐galactosamine
Activation of a murine macrophage cell line (RAW264.7) by PGN is mediated through the toll‐like receptor 2 (TLR2) signaling cascade, which involves the activation of a number of kinases, including p38 mitogen‐associated protein kinase (MAPK), extracellular signal‐regulated kinase (ERK) 1/2, inhibitor of NF-κB α (IκBα) and Akt [18,19]
Summary
Chloral hydrate is a well‐known sedative and anesthetic that is used in pediatric procedures, including echocardiograms and magnetic resonance imaging [1,2,3,4,5], and in animal experiments [6,7,8,9]. It was demonstrated that therapeutic concentrations of chloral hydrate delayed and reduced the magnitude of the inflammatory response and improved the survival rate of mice following the induction of liver injury with lipopolysaccharide and D‐galactosamine. This altered inflammatory response was associated with the inhibitory effects of chloral hydrate on nuclear factor‐κB (NF‐κB) activity and the levels of serum proinflammatory cytokines induced by lipopolysaccharide [13]. Activation of a murine macrophage cell line (RAW264.7) by PGN is mediated through the TLR2 signaling cascade, which involves the activation of a number of kinases, including p38 mitogen‐associated protein kinase (MAPK), extracellular signal‐regulated kinase (ERK) 1/2, inhibitor of NF-κB α (IκBα) and Akt [18,19]
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