Journal Article
Research Support, Non-U.S. Gov't
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Propofol reduces lipopolysaccharide-induced, NADPH oxidase (NOX 2) mediated TNF- α and IL-6 production in macrophages.

During an infection, lipopolysaccharide (LPS) stimulates the production of reactive oxygen species (ROS), which is mediated, in large part, by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs); NOX2 is the major NOX isoform found in the macrophage cell membrane. While the immunomodulatory activity of propofol is highly documented, its effect on the LPS-induced NOX2/ROS/NF-κB signaling pathway in macrophages has not been addressed. In present study, we used murine macrophage cell line RAW264.7 pretreated with propofol and stimulated with LPS. IL-6 and TNF-α expression, ROS production, and NOX activity were determined. Results showed that propofol attenuated LPS-induced TNF-α and IL-6 expression. Moreover, LPS-stimulated phosphorylation of NF-κB and generation of ROS were weakened in response to propofol. Propofol also reduced LPS-induced NOX activity and expression of gp91phox and p47phox. We conclude that propofol modulates LPS signaling in macrophages by reducing NOX-mediated production of TNF-α and IL-6.

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