期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 369, 期 3, 页码 868-872出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2008.02.132
关键词
alpha-tocopherol; ABCA1; ABCG1; CD36; LXR alpha; PPAR gamma; reverse cholesterol transport; atherosclerosis
Based on the oxidation hypothesis high closes of alpha-tocopherol have been advocated to prevent atherosclerosis, but clinical trials failed to demonstrate a benefit. As specific oxylipids activate PPAR gamma and LXR alpha, master regulators of lipid metabolism and cholesterol exporters, we hypothesized, that high dose alpha-tocopherol might interfere with reverse cholesterol transport out of the vessel wall. Human THP-1 cells, a foam cell model, were preincubated with alpha-tocopherol or carrier before exposure to oxidized LDL, delipidated HDL or control buffer. Specific mRNAs were quantified by real-time RT-PCR, LXR alpha activation by a reporter gene assay and cellular cholesterol homeostasis by oxLDL and dHDL facilitated uptake and efflux assays. alpha-Tocopherol significantly reduced baseline expression and stimulation by oxLDL of LXR alpha activity, CD36, ABCA1, and ABCG1. alpha-Tocopherol also reversed the suppression of CD36 and ABCA1 by dHDL. Thus alpha-Tocopherol compromises cellular lipid scavenging and channelling of cholesterol into reverse transport out of the vessel wall. (c) 2008 Elsevier Inc. All rights reserved.
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