Journal
TOXICOLOGY LETTERS
Volume 150, Issue 2, Pages 191-201Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2004.01.010
Keywords
retinoids; PGE2; COX-2; TNF-alpha; anti-inflammation
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Anti-inflammatory activity of retinoids has been demonstrated earlier, but their mechanism is poorly understood. In this study, we examined the effects of retinoids on lipopolysaccharide (LPS)-induced prostaglandin (PG) E-2 production, an indicator of cyclooxygenase (COX) activity, and COX-2 protein expression in mouse peritoneal macrophages, and tumor necrosis factor (TNF)-alpha release in rat peripheral blood mononuclear cell (PBMC) to elucidate their possible mechanism for anti-inflammation. All-trans retinoic acid (t-RA) and all-trans retinol significantly inhibited a LPS-induced PGE(2) production as assessed by enzyme-linked immunosorbant assay (ELISA) and COX-2 protein expression as assessed by Western blot assay in mouse peritoneal macrophages, after knocking out the COX-1 activity by aspirin. All-trans retinoic acid, but not all-trans retinol, inhibited LPS-induced TNF-alpha. release as assessed by ELISA in rat PBMC. These findings suggest that the modulation of COX-2 and TNF-alpha release could be one of the possible pathways by which retinoids function as anti-inflammatory agents. (C) 2004 Elsevier Ireland Ltd. All rights reserved.
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