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Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 325481, 9 pages
http://dx.doi.org/10.1155/2013/325481
Research Article

Propofol Reduces Lipopolysaccharide-Induced, NADPH Oxidase (NOX2) Mediated TNF-α and IL-6 Production in Macrophages

1Department of Anesthesiology, Qilu Hospital of Shandong University, Shandong University, No. 107 Wen Hua Xi Road, Jinan, Shandong 250012, China
2Department of Pathogeny Biology, Shandong University School of Medicine, No. 44 Wen Hua Xi Road, Jinan, Shandong 250012, China
3Department of Cardiology, Qilu Hospital of Shandong University, Shandong University, No. 107 Wen Hua Xi Road, Jinan, Shandong 250012, China

Received 26 August 2013; Revised 11 October 2013; Accepted 13 October 2013

Academic Editor: Eirini I. Rigopoulou

Copyright © 2013 Tao Meng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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- B 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- expression, ROS production, and NOX activity were determined. Results showed that propofol attenuated LPS-induced TNF- and IL-6 expression. Moreover, LPS-stimulated phosphorylation of NF- B 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- and IL-6.