期刊
FASEB JOURNAL
卷 30, 期 8, 页码 2792-2801出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.201500155R
关键词
metabololipidomics; resolvins; lipoxins; n-3 fatty acids; inflammation
资金
- U.S. National Institutes of Health (NIH) National Institute of General Medical Sciences [P01GM095467, RO1GM03865]
- NIH National Heart, Lung, and Blood Institute [P50HL083813]
Inflammation in arterial walls leads to coronary artery disease (CAD). Because specialized proresolving lipid mediators (SPMs; lipoxins, resolvins, and protectins) stimulate resolution of inflammation in animal models, we tested whether n-3 fatty acids impact SPM profiles in patients with CAD and promote clot remodeling. Six patients with stable CAD were randomly assigned to either treatment with daily 3.36 g Lovaza for 1 yr or without. Targeted lipid mediator-metabololipidomics showed that both groups had absence of resolvin D1 (RvD1), RvD2, RvD3, RvD5 and resolvin E1-all of which are present in healthy patients. Those not taking Lovaza had an absence of aspirin-triggered resolvin D3 (AT-RvD3) and aspirin-triggered lipoxin B-4 (AT-LXB4). Lovaza treatment restored AT-RvD3 and AT-LXB4 and gave levels of RvD6 and aspirin-triggered protectin D1(AT-PD1) twice as high (resolvin E2 similar to 5 fold) as well as lower prostaglandins. Principal component analysis indicated positive relationships for patients with CAD who were receiving Lovaza with increased AT-RvD3, RvD6, AT-PD1, and AT-LXB4. SPMs identified in Lovaza-treated patients with CAD enhanced similar to 50% at 1 nM macrophage uptake of blood clots. These results indicate that patients with CAD have lower levels and/or absence of specific SPMs that were restored with Lovaza; these SPMs promote macrophage phagocytosis of blood clots. Together, they suggest that low vascular SPMs may enable progression of chronic vascular inflammation predisposing to coronary atherosclerosis and to thrombosis.
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