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Allicin induces the upregulation of ABCA1 expression via PPARγ/LXRα signaling in THP-1 macrophage-derived foam cells

Allicin is considered anti-atherosclerotic due to its antioxidant and anti-inflammatory effects, which makes it an important drug for the prevention and treatment of atherosclerosis. However, the effects of allicin on foam cells are unclear. Thus, in this study, we examined the effects of allicin on...

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Autores principales: Lin, Xiao-Long, Hu, Hui-Jun, Liu, Yuan-Bo, Hu, Xue-Mei, Fan, Xiao-Juan, Zou, Wei-Wen, Pan, Yong-Quan, Zhou, Wen-Quan, Peng, Min-Wen, Gu, Cai-Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5428973/
https://www.ncbi.nlm.nih.gov/pubmed/28440421
http://dx.doi.org/10.3892/ijmm.2017.2949
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author Lin, Xiao-Long
Hu, Hui-Jun
Liu, Yuan-Bo
Hu, Xue-Mei
Fan, Xiao-Juan
Zou, Wei-Wen
Pan, Yong-Quan
Zhou, Wen-Quan
Peng, Min-Wen
Gu, Cai-Hong
author_facet Lin, Xiao-Long
Hu, Hui-Jun
Liu, Yuan-Bo
Hu, Xue-Mei
Fan, Xiao-Juan
Zou, Wei-Wen
Pan, Yong-Quan
Zhou, Wen-Quan
Peng, Min-Wen
Gu, Cai-Hong
author_sort Lin, Xiao-Long
collection PubMed
description Allicin is considered anti-atherosclerotic due to its antioxidant and anti-inflammatory effects, which makes it an important drug for the prevention and treatment of atherosclerosis. However, the effects of allicin on foam cells are unclear. Thus, in this study, we examined the effects of allicin on lipid accumulation via peroxisome proliferator-activated receptor γ (PPARγ)/liver X receptor α (LXRα) in THP-1 macrophage-derived foam cells. THP-1 cells were exposed to 100 nM phorbol myristate acetate (PMA) for 24 h, and then to oxydized low-density lipoprotein (ox-LDL; 50 mg/ml) to induce foam cell formation. The results of Oil Red O staining and high-performance liquid chromatography (HPLC) revealed showed that pre-treatment of the foam cells with allicin decreased total cholesterol, free cholesterol (FC) and cholesterol ester levels in cells, and also decreased lipid accumulation. Moreover, allicin upregulated ATP binding cassette transporter A1 (ABCA1) expression and promoted cholesterol efflux. However, these effects were significantly abolished by transfection with siRNA targeting ABCA1. Furthermore, PPARγ/LXRα signaling was activated by allicin treatment. The allicin-induced upregulation of ABCA1 expression was also abolished by PPARγ inhibitor (GW9662) and siRNA or LXRα siRNA co-treatment. Overall, our data demonstrate that the allicin-induced upregulation of ABCA1 promotes cholesterol efflux and reduces lipid accumulation via PPARγ/LXRα signaling in THP-1 macrophage-derived foam cells.
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spelling pubmed-54289732017-05-15 Allicin induces the upregulation of ABCA1 expression via PPARγ/LXRα signaling in THP-1 macrophage-derived foam cells Lin, Xiao-Long Hu, Hui-Jun Liu, Yuan-Bo Hu, Xue-Mei Fan, Xiao-Juan Zou, Wei-Wen Pan, Yong-Quan Zhou, Wen-Quan Peng, Min-Wen Gu, Cai-Hong Int J Mol Med Articles Allicin is considered anti-atherosclerotic due to its antioxidant and anti-inflammatory effects, which makes it an important drug for the prevention and treatment of atherosclerosis. However, the effects of allicin on foam cells are unclear. Thus, in this study, we examined the effects of allicin on lipid accumulation via peroxisome proliferator-activated receptor γ (PPARγ)/liver X receptor α (LXRα) in THP-1 macrophage-derived foam cells. THP-1 cells were exposed to 100 nM phorbol myristate acetate (PMA) for 24 h, and then to oxydized low-density lipoprotein (ox-LDL; 50 mg/ml) to induce foam cell formation. The results of Oil Red O staining and high-performance liquid chromatography (HPLC) revealed showed that pre-treatment of the foam cells with allicin decreased total cholesterol, free cholesterol (FC) and cholesterol ester levels in cells, and also decreased lipid accumulation. Moreover, allicin upregulated ATP binding cassette transporter A1 (ABCA1) expression and promoted cholesterol efflux. However, these effects were significantly abolished by transfection with siRNA targeting ABCA1. Furthermore, PPARγ/LXRα signaling was activated by allicin treatment. The allicin-induced upregulation of ABCA1 expression was also abolished by PPARγ inhibitor (GW9662) and siRNA or LXRα siRNA co-treatment. Overall, our data demonstrate that the allicin-induced upregulation of ABCA1 promotes cholesterol efflux and reduces lipid accumulation via PPARγ/LXRα signaling in THP-1 macrophage-derived foam cells. D.A. Spandidos 2017-06 2017-04-11 /pmc/articles/PMC5428973/ /pubmed/28440421 http://dx.doi.org/10.3892/ijmm.2017.2949 Text en Copyright: © Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Lin, Xiao-Long
Hu, Hui-Jun
Liu, Yuan-Bo
Hu, Xue-Mei
Fan, Xiao-Juan
Zou, Wei-Wen
Pan, Yong-Quan
Zhou, Wen-Quan
Peng, Min-Wen
Gu, Cai-Hong
Allicin induces the upregulation of ABCA1 expression via PPARγ/LXRα signaling in THP-1 macrophage-derived foam cells
title Allicin induces the upregulation of ABCA1 expression via PPARγ/LXRα signaling in THP-1 macrophage-derived foam cells
title_full Allicin induces the upregulation of ABCA1 expression via PPARγ/LXRα signaling in THP-1 macrophage-derived foam cells
title_fullStr Allicin induces the upregulation of ABCA1 expression via PPARγ/LXRα signaling in THP-1 macrophage-derived foam cells
title_full_unstemmed Allicin induces the upregulation of ABCA1 expression via PPARγ/LXRα signaling in THP-1 macrophage-derived foam cells
title_short Allicin induces the upregulation of ABCA1 expression via PPARγ/LXRα signaling in THP-1 macrophage-derived foam cells
title_sort allicin induces the upregulation of abca1 expression via pparγ/lxrα signaling in thp-1 macrophage-derived foam cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5428973/
https://www.ncbi.nlm.nih.gov/pubmed/28440421
http://dx.doi.org/10.3892/ijmm.2017.2949
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