Document Detail


Eicosapentaenoic acid administration attenuates the pro-inflammatory properties of VLDL by decreasing its susceptibility to lipoprotein lipase in macrophages.
MedLine Citation:
PMID:  22018640     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
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.
Authors:
Yasutaka Jinno; Masanori Nakakuki; Hiroyuki Kawano; Tatsuto Notsu; Kiyoshi Mizuguchi; Kazunori Imada
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-10-4
Journal Detail:
Title:  Atherosclerosis     Volume:  -     ISSN:  1879-1484     ISO Abbreviation:  -     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-10-24     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0242543     Medline TA:  Atherosclerosis     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
Affiliation:
Development Research, Pharmaceutical Research Center, Mochida Pharmaceutical Co., Ltd., 722 Jimba-aza-Uenohara, Gotemba, Shizuoka 412-8524, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Seasonal and socio-demographic predictors of suicide in Ireland: A 22year study.
Next Document:  Atorvastatin increases exercise leg blood flow in healthy adults.