Effect of retinoids on LPS-induced COX-2 expression and COX-2 associated PGE2 release from mouse peritoneal macrophages and TNF-α release from rat peripheral blood mononuclear cells

Abstract 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)-α 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-α release as assessed by ELISA in rat PBMC. These findings suggest that the modulation of COX-2 and TNF-α release could be one of the possible pathways by which retinoids function as anti-inflammatory agents.