| Eicosapentaenoic acid administration attenuates the pro-inflammatory properties of VLDL by decreasing its susceptibility to lipoprotein lipase in macrophages. | |
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MedLine Citation:
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PMID: 22018640 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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High level of plasma very low-density lipoprotein (VLDL) has been identified as a risk factor for coronary heart disease. Recent evidence suggests that excess VLDL induces inflammatory responses in macrophages and vascular endothelial cells. The Japan EPA Lipid Intervention Study (JELIS), a large scale clinical trial, demonstrated that highly purified eicosapentaenoic acid (EPA) prevented the onset of cardiovascular events in LDL-cholesterol independent fashion. In this study, we investigated the impact of EPA on pro-inflammatory properties of VLDL. Effects of VLDL prepared from mice fed 5% EPA diet for 1 week (EPA-VLDL) or mice fed normal diet (Ctrl-VLDL) on the mRNA expression of pro-inflammatory factors were examined in human THP-1 macrophages. Ctrl-VLDL increased mRNA expression of pro-inflammatory factors such as interleukin-1β and tumor necrosis factor-α in macrophages. In contrast, the increases in pro-inflammatory factors by EPA-VLDL were lower than those by Ctrl-VLDL. Moreover, EPA-VLDL-treated macrophages had less triglyceride accumulation than Ctrl-VLDL-treated macrophages. Inhibition of lipoprotein lipase (LPL) appeared to suppress inflammation and triglyceride accumulation by Ctrl-VLDL suggesting that hydrolysis of VLDL is required for the pro-inflammatory properties of VLDL. Free fatty acid release from EPA-VLDL by macrophages and purified LPL was less than that from Ctrl-VLDL. Extracellular LPL mass was decreased by EPA-VLDL. Taken together, these findings indicate that the pro-inflammatory properties of VLDL were attenuated by EPA administration via decrease in susceptibility of VLDL to LPL. It appears possible that anti-inflammatory effects of EPA on VLDL contribute to the suppression of cardiovascular risk by EPA. |
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Authors:
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Yasutaka Jinno; Masanori Nakakuki; Hiroyuki Kawano; Tatsuto Notsu; Kiyoshi Mizuguchi; Kazunori Imada |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-10-4 |
Journal Detail:
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Title: Atherosclerosis Volume: - ISSN: 1879-1484 ISO Abbreviation: - Publication Date: 2011 Oct |
Date Detail:
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Created Date: 2011-10-24 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0242543 Medline TA: Atherosclerosis Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2011 Elsevier Ireland Ltd. All rights reserved. |
Affiliation:
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Development Research, Pharmaceutical Research Center, Mochida Pharmaceutical Co., Ltd., 722 Jimba-aza-Uenohara, Gotemba, Shizuoka 412-8524, Japan. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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