Curcumin Enhanced Cholesterol Efflux by Upregulating ABCA1 Expression Through AMPK-SIRT1-LXRα Signaling in THP-1 Macrophage-Derived Foam Cells
Autor: | Hong-ru Feng, Zuo Wang, Yongquan Pan, Xiao-Juan Fan, Wei-Wen Zou, Huijun Hu, Mi-Hua Liu, Xue-Mei Hu, Xiaolong Lin |
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Rok vydání: | 2015 |
Předmět: |
Small interfering RNA
Curcumin Cell Survival Cell Line chemistry.chemical_compound Sirtuin 1 Genetics Humans Liver X receptor Protein kinase A Molecular Biology Hypolipidemic Agents Liver X Receptors biology Adenylate Kinase AMPK Cell Differentiation Lipid metabolism Cell Biology General Medicine Orphan Nuclear Receptors Up-Regulation Cell biology Cholesterol chemistry ABCA1 biology.protein lipids (amino acids peptides and proteins) Signal transduction ATP Binding Cassette Transporter 1 Foam Cells Signal Transduction |
Zdroj: | DNA and Cell Biology. 34:561-572 |
ISSN: | 1557-7430 1044-5498 |
Popis: | 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. |
Databáze: | OpenAIRE |
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