Modulation of monocyte-macrophage function with α-tocopherol:: Implications for atherosclerosis

被引:17
作者
Devaraj, S [1 ]
Harris, A
Jialal, I
机构
[1] Univ Texas, SW Med Ctr, Dept Pathol, Dallas, TX 75390 USA
[2] Univ Texas, SW Med Ctr, Dept Internal Med, Dallas, TX 75390 USA
[3] Univ Texas, SW Med Ctr, Dept Pathol, Dallas, TX 75390 USA
关键词
cardiovascular disease; antioxidants; platelet aggregation; alpha-tocopherol;
D O I
10.1301/002966402760240381
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Cardiovascular disease is the leading cause of morbidity and mortality in the Western world. Monocyte-macrophages are crucial cells in atherogenesis. Several lines of evidence suggest that antioxidants, especially alpha-tocopherol, have beneficial effects with regard to cardiovascular disease. alpha-Tocopherol has beneficial effects on cell functions that are pivotal in atherogenesis. alpha-Tocopherol inhibits platelet aggregation and proinflammatory activity of monocytes. In vitro data also support an effect of alpha-tocopherol on smooth muscle cell proliferation and endothelial function. Finally, recent data support an effect of alpha-tocopherol on macrophage function. The mounting evidence from in vitro and in vivo studies provides a sound scientific basis for alpha-tocopherol supplementation. Further clinical trials are required, however, before a definitive recommendation can be made for primary and secondary prevention of heart disease.
引用
收藏
页码:8 / 14
页数:7
相关论文
共 48 条
[1]   LEUKOCYTE-ENDOTHELIAL INTERACTIONS AND REGULATION OF LEUKOCYTE MIGRATION [J].
ADAMS, DH ;
SHAW, S .
LANCET, 1994, 343 (8901) :831-836
[2]   INHIBITION OF IL-1-BETA EXPRESSION IN THP-1 CELLS BY PROBUCOL AND TOCOPHEROL [J].
AKESON, AL ;
WOODS, CW ;
MOSHER, LB ;
THOMAS, CE ;
JACKSON, RL .
ATHEROSCLEROSIS, 1991, 86 (2-3) :261-270
[3]  
[Anonymous], AM J CLIN NUTR
[4]   PREVENTION OF CHOLESTERYL ESTER ACCUMULATION IN P388D(1) MACROPHAGE-LIKE CELLS BY INCREASED CELLULAR VITAMIN-E DEPENDS ON SPECIES OF EXTRACELLULAR CHOLESTEROL - CONVENTIONAL HETEROLOGOUS NONHUMAN CELL-CULTURES ARE POOR MODELS OF HUMAN ATHEROSCLEROTIC FOAM CELL-FORMATION [J].
ASMIS, R ;
LLORENTE, VC ;
GEY, KF .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1995, 233 (01) :171-178
[5]   Vitamin E supplementation of human macrophages prevents neither foam cell formation nor increased susceptibility of foam cells to lysis by oxidized LDL [J].
Asmis, R ;
Jelk, J .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2000, 20 (09) :2078-2086
[6]   Molecular basis of α-tocopherol control of smooth muscle cell proliferation [J].
Azzi, Angelo ;
Aratri, Elisabetta ;
Boscoboinik, Daniel ;
Clement, Sophie ;
Ozer, Nesrin K. ;
Ricciarelli, Roberta ;
Spycher, Stefan .
BIOFACTORS, 1998, 7 (1-2) :3-14
[7]  
Baoutina A, 1998, J LIPID RES, V39, P114
[8]   ATHEROSCLEROSIS - BASIC MECHANISMS - OXIDATION, INFLAMMATION, AND GENETICS [J].
BERLINER, JA ;
NAVAB, M ;
FOGELMAN, AM ;
FRANK, JS ;
DEMER, LL ;
EDWARDS, PA ;
WATSON, AD ;
LUSIS, AJ .
CIRCULATION, 1995, 91 (09) :2488-2496
[9]  
BEVILACQUA MP, 1984, J EXP MED, V163, P1595
[10]   Decreased lesion formation in CCR2-/- mice reveals a role for chemokines in the initiation of atherosclerosis [J].
Boring, L ;
Gosling, J ;
Cleary, M ;
Charo, IF .
NATURE, 1998, 394 (6696) :894-897