Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2010, Article ID 293642, 5 pages
http://dx.doi.org/10.1155/2010/293642
Research Article

Suppression of Inflammatory Mediators by Cruciferous Vegetable-Derived Indole-3-Carbinol and Phenylethyl Isothiocyanate in Lipopolysaccharide-Activated Macrophages

1Department of Radiation Oncology, Taipei Municipal Wan-Fang Hospital, Taipei Medical University, Taipei 116, Taiwan
2School of Nutrition and Health Sciences, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan

Received 11 December 2009; Revised 27 January 2010; Accepted 9 February 2010

Academic Editor: Changlin Li

Copyright © 2010 Jo-Ting Tsai 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

This study was aimed to examine the effects of indole-3-carbinol (I3C) and -phenylethyl isothiocyanate (PEITC), bioactive components present in cruciferous vegetable, on the production of inflammatory mediators, including nitric oxide (NO), tumor necrosis factor- (TNF- ) and interleukin-10 (IL-10), in lipopolysaccharide- (LPS-) stimulated RAW 264.7 macrophages. Possible mechanisms of the NO-inhibitory effects were also explored. The results indicated that I3C and PEITC inhibited NO production, and this suppression was associated with decreased production of TNF- and IL-10 by activated macrophages. In addition, I3C suppressed NO production even after the inducible nitric oxide synthase (iNOS) protein had been produced, but such an inhibitory effect was not observed in cells treated with PEITC. Furthermore, both compounds reduced the NO contents generated from an NO donor in a cell-free condition, suggesting that the increased NO clearance may have contributed to the NO-inhibitory effects. In summary, both I3C and PEITC possessed antiinflammatory effects by inhibiting the productions of NO, TNF- , and IL-10, although the NO-inhibitory effects may have involved in different mechanisms.