Anti-inflammatory effects of tocopherol metabolites

Our objective was to assess the anti-inflammatory effects of α-tocopherol, γ-tocopherol, and their metabolites 2,5,7,8-tetramethyl-2-(β-carboxyethyl)-6-hydroxychroman (α-CEHC) and 2,7,8-trimethyl-2-(β-carboxyethyl)-6-hydroxychroman (γ-CEHC) in defined cell culture systems. Rat aortic endothelial cells and mouse microglial cultures were treated with tumor necrosis factor TNFα or bacterial lipopolysaccharide (LPS) and nitrite and prostaglandin E2 (PGE2) were measured. α-CEHC suppressed TNFα-stimulated nitrite production in both cell types, whereas both CEHC derivatives inhibited LPS-stimulated microglial nitrite efflux. Both α-CEHC and γ-CEHC inhibited microglial PGE2 production, but neither α- nor γ-tocopherol was effective at inhibiting cytokine-stimulated inflammatory processes. These results show that the anti-inflammatory effects of tocopherols are highly cell type-, stimulus-, and endpoint-dependent.