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DNA Cell Biol ; 34(9): 561-72, 2015 Sep.
Article in English | MEDLINE | ID: mdl-26102194

ABSTRACT

Curcumin, a traditional Chinese derivative from the rhizomes of Curcuma longa, is beneficial to health by modulating lipid metabolism and suppressing atherogenesis. A key part of atherosclerosis is the failure of macrophages to restore their cellular cholesterol homeostasis and the formation of foam cells. In this study, results showed that curcumin dramatically increased the expression of ATP-binding cassette transporter 1 (ABCA1), promoted cholesterol efflux from THP-1 macrophage-derived foam cells, and reduced cellular cholesterol levels. Curcumin activated AMP-activated protein kinase (AMPK) and SIRT1, and then activated LXRα in THP-1 macrophage-derived foam cells. Inhibiting AMPK/SIRT1 activity by its specific inhibitor or by small interfering RNA could inhibit LXRα activation and abolish curcumin-induced ABCA1 expression and cholesterol efflux. Thus, curcumin enhanced cholesterol efflux by upregulating ABCA1 expression through activating AMPK-SIRT1-LXRα signaling in THP-1 macrophage-derived foam cells. This study describes a possible mechanism for understanding the antiatherogenic effects of curcumin on attenuating the progression of atherosclerosis.


Subject(s)
ATP Binding Cassette Transporter 1/metabolism , Cholesterol/metabolism , Curcumin/pharmacology , Foam Cells/metabolism , Hypolipidemic Agents/pharmacology , ATP Binding Cassette Transporter 1/genetics , Adenylate Kinase/metabolism , Cell Differentiation , Cell Line , Cell Survival/drug effects , Foam Cells/drug effects , Humans , Liver X Receptors , Orphan Nuclear Receptors/metabolism , Signal Transduction , Sirtuin 1/metabolism , Up-Regulation
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