Anti-inflammatory effects of tocopherol metabolites

Biochem Biophys Res Commun. 2004 Jul 2;319(3):1047-52. doi: 10.1016/j.bbrc.2004.05.082.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Antioxidants / pharmacology*
  • Cells, Cultured
  • Dinoprostone / metabolism
  • Dose-Response Relationship, Drug
  • Endothelial Cells / cytology
  • Endothelial Cells / drug effects*
  • Endothelial Cells / metabolism
  • Lipopolysaccharides / pharmacology
  • Mice
  • Microglia / cytology
  • Microglia / drug effects*
  • Microglia / metabolism
  • Nitrites / metabolism
  • Rats
  • Tocopherols / pharmacology*
  • Tumor Necrosis Factor-alpha / pharmacology


  • Anti-Inflammatory Agents
  • Antioxidants
  • Lipopolysaccharides
  • Nitrites
  • Tumor Necrosis Factor-alpha
  • Dinoprostone
  • Tocopherols