1. Anti-inflammatory effects of tocopherol metabolites.
- Author
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Grammas P, Hamdheydari L, Benaksas EJ, Mou S, Pye QN, Wechter WJ, Floyd RA, Stewart C, and Hensley K
- Subjects
- Animals, Cells, Cultured, Dinoprostone metabolism, Dose-Response Relationship, Drug, Endothelial Cells cytology, Endothelial Cells metabolism, Lipopolysaccharides pharmacology, Mice, Microglia cytology, Microglia metabolism, Nitrites metabolism, Rats, Tumor Necrosis Factor-alpha pharmacology, Anti-Inflammatory Agents pharmacology, Antioxidants pharmacology, Endothelial Cells drug effects, Microglia drug effects, Tocopherols pharmacology
- Abstract
Our objective was to assess the anti-inflammatory effects of alpha-tocopherol, gamma-tocopherol, and their metabolites 2,5,7,8-tetramethyl-2-(beta-carboxyethyl)-6-hydroxychroman (alpha-CEHC) and 2,7,8-trimethyl-2-(beta-carboxyethyl)-6-hydroxychroman (gamma-CEHC) in defined cell culture systems. Rat aortic endothelial cells and mouse microglial cultures were treated with tumor necrosis factor TNFalpha or bacterial lipopolysaccharide (LPS) and nitrite and prostaglandin E(2) (PGE(2)) were measured. alpha-CEHC suppressed TNFalpha-stimulated nitrite production in both cell types, whereas both CEHC derivatives inhibited LPS-stimulated microglial nitrite efflux. Both alpha-CEHC and gamma-CEHC inhibited microglial PGE(2) production, but neither alpha- nor gamma-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.
- Published
- 2004
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