Quercetin up-regulates expressions of peroxisome proliferator-activated receptor gamma, liver X receptor alpha, and ATP binding cassette transporter A1 genes and increases cholesterol efflux in human macrophage cell line
- Authors
- Lee, Seung-Min; Moon, Jiyoung; Cho, Yoonsu; Chung, Ji Hyung; Shin, Min-Jeong
- Issue Date
- 2월-2013
- Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
- Keywords
- Quercetin; HDL; apoA1; ABCA1; PPAR gamma; LXR alpha
- Citation
- NUTRITION RESEARCH, v.33, no.2, pp.136 - 143
- Indexed
- SCIE
SCOPUS
- Journal Title
- NUTRITION RESEARCH
- Volume
- 33
- Number
- 2
- Start Page
- 136
- End Page
- 143
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/104060
- DOI
- 10.1016/j.nutres.2012.11.010
- ISSN
- 0271-5317
- Abstract
- Cholesterol-laden macrophages trigger accumulation of foam cells and increase the risk of developing atherosclerosis. We hypothesized that quercetin could lower the content of cholesterol in macrophages by regulating the expression of the ATP binding cassette transporter A1 (ABCA1) gene in differentiated human acute monocyte leukemia cell line (THP-1) cells and thereby reducing the chance of forming foam cells. Quercetin, in concentrations up to 30 mu M, was not cytotoxic to differentiated THP-1 cells. Quercetin up-regulated both ABCA1 messenger RNA and protein expression in differentiated THP-1 cells, and its maximum effects were demonstrated at 0.3 mu M for 4 to 8 hours in incubation. In addition, quercetin increased protein levels of peroxisome proliferator-activated receptor gamma (PPAR gamma) and liver X receptor alpha (LXR alpha) within 2 hours of treatment. Because PPAR gamma and LXR alpha are important transcriptional factors for ABCA1, quercetin-induced up-regulation of ABCA1 maybe mediated by increased expression levels of the PPAR gamma and LXR alpha genes. Furthermore, quercetin-enhanced cholesterol efflux from differentiated THP-1 cells to both high-density lipoprotein (HDL) and apolipoprotein A1. Quercetin at the dose of 0.15 mu M elevated the cholesterol efflux only for HDL. At the dose of 0.3 mu M, quercetin demonstrated effects both on HDL and apolipoprotein A1. Our data demonstrated that quercetin increased the expressions of PPAR gamma, LXR alpha, and ABCA1 genes and cholesterol efflux from THP-1 macrophages. Quercetin-induced expression of PPAR gamma and LXR alpha might subsequently affect up-regulation of their target gene ABCA1. Taken together, ingestion of quercetin or quercetin-rich foods could be an effective way to improve cholesterol efflux from macrophages, which would contribute to lowering the risk of atherosclerosis. (c) 2013 Elsevier Inc. All rights reserved.
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