Abstract:
: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.
journal_name
Atherosclerosisjournal_title
Atherosclerosisauthors
Jinno Y,Nakakuki M,Kawano H,Notsu T,Mizuguchi K,Imada Kdoi
10.1016/j.atherosclerosis.2011.09.046subject
Has Abstractpub_date
2011-12-01 00:00:00pages
566-72issue
2eissn
0021-9150issn
1879-1484pii
S0021-9150(11)00952-Xjournal_volume
219pub_type
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