Anti-inflammatory effects of tocopherol metabolites

被引：85

作者：

Grammas, P

Hamdheydari, L

Benaksas, EJ

Mou, S

Pye, QN

Wechter, WJ

Floyd, RA

Stewart, C

Hensley, K ^{[1
]}

机构：

[1] Univ Oklahoma, Hlth Sci Ctr, Ctr Neurosci, Oklahoma City, OK 73104 USA

[2] Oklahoma Med Res Fdn, Free Radical Biol & Aging Res Program, Oklahoma City, OK 73104 USA

[3] Univ Oklahoma, Hlth Sci Ctr, Dept Pathol, Oklahoma City, OK 73104 USA

[4] Encore Pharmaceut Inc, Riverside, CA 92507 USA

[5] Univ Oklahoma, Hlth Sci Ctr, Dept Biochem, Oklahoma City, OK 73104 USA

[6] Univ Oklahoma, Hlth Sci Ctr, Dept Cell Biol, Oklahoma City, OK 73104 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2004年 / 319卷 / 03期

关键词：

alpha-tocopherol; gamma-tocopherol; carboxyethylhydroxychroman; microglia; endothelial; inflammation;

D O I：

10.1016/j.bbrc.2004.05.082

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

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 PGE2 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. (C) 2004 Elsevier Inc. All rights reserved.

引用

页码：1047 / 1052

页数：6

共 28 条

[1]

Tocopherols are metabolized in HepG2 cells by side chain ω-oxidation and consecutive β-oxidation [J].