Evidence for inhibition of nitric oxide and inducible nitric oxide synthase in Caco-2 and RAW 264.7 cells by a Maillard reaction product [5-(5,6-dihydro-4H-pyridin-3-ylidenemethyl)furan-2-yl]-methanol.

We have recently isolated and characterized the chemical structure of a bioactive Maillard reaction product, [5-(5,6-dihydro-4H-pyridin-3-ylidenemethyl)furan-2-yl]-methanol (F3-A), from an aqueous glucose (Glc) and lysine (Lys) Maillard reaction (MR) model system. Here, we investigate further the mechanisms for anti-inflammatory effects of this product in Caco-2 and RAW 264.7 cells. The anti-inflammatory capacity of F3-A recovered from Glc-Lys MR mixture and a synthesized product were compared with those of the specific inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (AG), and the nuclear factor-kappa B (NF-κB) inhibitor, pyrrolidine dithiocarbamate (PDTC). F3-A produced a dose-dependent inhibition of extracellular nitric oxide (NO) production and iNOS translation in Caco-2 cells induced with interferon gamma (IFN-γ) and phorbol 12-myristate 13-acetate (PMA), and these effects were more potent than those obtained with AG. Moreover, a combination of F3-A and AG to attenuate intestinal inflammation was additive. However, F3-A inhibited only intracellular NO production in RAW 264.7 cells and did not inhibit COX-2 or NF-κB in either cell line. We conclude that the anti-inflammatory properties of F3-A are cell specific, working through different mechanism between macrophages and intestinal cells.