P19 THE OMEGA 3 POLYUNSATURATED FATTY ACID, EICOSAPENTAENOIC ACID INHIBITS FOAM CELL FORMATION AND SECRETION OF PRO-INFLAMMATORY MEDIATORS

2018 ◽  
Vol 114 (suppl_2) ◽  
pp. S7-S7
Author(s):  
D R Lezama ◽  
M Chimen ◽  
A J Iqbal ◽  
G E Rainger
Keyword(s):  
Fatty Acid ◽  
Eicosapentaenoic Acid ◽  
Polyunsaturated Fatty Acid ◽  
Inflammatory Mediators ◽  
Foam Cell ◽  
Cell Formation ◽  
Foam Cell Formation ◽  
Omega 3

scholarly journals TR4 nuclear receptor functions as a fatty acid sensor to modulate CD36 expression and foam cell formation

2009 ◽  
Vol 106 (32) ◽  
pp. 13353-13358 ◽  
Author(s):  
S. Xie ◽  
Y.-F. Lee ◽  
E. Kim ◽  
L.-M. Chen ◽  
J. Ni ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Nuclear Receptor ◽  
Foam Cell ◽  
Cell Formation ◽  
Foam Cell Formation ◽  
Cd36 Expression

Anticolorectal cancer activity of the omega-3 polyunsaturated fatty acid eicosapentaenoic acid

Gut ◽  
2014 ◽  
Vol 63 (11) ◽  
pp. 1760-1768 ◽  
Author(s):  
Andrew J Cockbain ◽  
Milene Volpato ◽  
Amanda D Race ◽  
Alessandra Munarini ◽  
Chiara Fazio ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Eicosapentaenoic Acid ◽  
Polyunsaturated Fatty Acid ◽  
Omega 3 ◽  
Cancer Activity

Activation of Inflammatory Mediators and Potential Role of Ah-Receptor Ligands in Foam Cell Formation

2004 ◽  
Vol 4 (4) ◽  
pp. 363-374 ◽  
Author(s):  
Christoph F. A. Vogel ◽  
Eric Sciullo ◽  
Fumio Matsumura
Keyword(s):  
Inflammatory Mediators ◽  
Potential Role ◽  
Foam Cell ◽  
Cell Formation ◽  
Ah Receptor ◽  
Foam Cell Formation ◽  
Receptor Ligands

scholarly journals Overexpression of NF-κB p65 in macrophages ameliorates atherosclerosis in apoE-knockout mice

2013 ◽  
Vol 305 (11) ◽  
pp. E1375-E1383 ◽  
Author(s):  
Xin Ye ◽  
Xiaoting Jiang ◽  
Wei Guo ◽  
Katie Clark ◽  
Zhanguo Gao
Keyword(s):  
Fatty Acid ◽  
Energy Expenditure ◽  
Knockout Mice ◽  
Foam Cell ◽  
Cell Formation ◽  
Atherosclerotic Lesion ◽  
Foam Cell Formation ◽  
Acid Oxidation ◽  
Fatty Acid Binding ◽  
Apoe Knockout Mice

The transcription factor NF-κB p65 is a key regulator in the regulation of an inflammatory response and in the pathology of atherosclerosis. However, there is no direct evidence for the role of NF-κB in macrophages in the development of atherosclerosis. We investigated whether macrophage overexpression of p65 in apoE-knockout mice could improve atherosclerosis. Transgenic (Tg) mice overexpressing p65 in macrophages were generated by crossing fatty acid-binding protein 4 (aP2) promoter-controlled p65 mice with apoE-knockout (KO) mice. Tg mice exhibited functional activation of NF-κB signaling in macrophages and fat tissues. We observed that the atherosclerotic lesion was 40% less in the Tg mice compared with the apoE-KO controls fed a standard atherogenic diet for 16 wk ( n = 12). The Tg mice were leaner from reduced fat mass by increased energy expenditure. Moreover, the overexpression of p65 in macrophages suppressed foam cell formation. Our results show that there is 1) an increased fatty acid oxidation in macrophages, 2) a reduced scavenger receptor CD36 expression and lipid accumulation in microphages, 3) reduced-inflammation cytokines in serum, and 4) enhanced energy expenditure in Tg mice. Our data suggest that activation of NF-κB in macrophages has atheroprotective effects in mice by enhancing lipid metabolism and energy expenditure.

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