NF-kappaB Inhibitors that Prevent Foam Cell Formation and Atherosclerotic Plaque Accumulation

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Anthony Dellinger (Creator)
Christopher Kepley, Associate Professor (Creator)
The University of North Carolina at Greensboro (UNCG )
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Abstract: The transformation of monocyte-derived macrophages into lipid-laden foam cells is one inflammatory process underlying atherosclerotic disease. Previous studies have demonstrated that fullerene derivatives (FDs) have inflammation-blunting properties. Thus, it was hypothesized that FD could inhibit the transformation process underlying foam cell formation. Fullerene derivatives inhibited the phorbol myristic acid/oxidized low-density lipoprotein-induced differentiation of macrophages into foam cells as determined by lipid staining and morphology. Lipoprotein-induced generation of TNF-a, C5a-induced MC activation, ICAM-1 driven adhesion, and CD36 expression were significantly inhibited in FD treated cells compared to non-treated cells. Inhibition appeared to be mediated through the NF-kappaB pathway as FD reduced expression of NF-kappaB and atherosclerosis-associated genes. Compared to controls, FD dramatically inhibited plaque formation in arteries of apolipoprotein E null mice. Thus, FD may be an unrecognized therapy to prevent atherosclerotic lesions via inhibition of foam cell formation and MC stabilization.

Additional Information

Nanomedicine: Nanotechnology, Biology and Medicine, 2017 Aug;13(6):2037-2048
Language: English
Date: 2017
Atherosclerosis, NF-kappaB, Foam cells, Fullerenes, Low-density lipoprotein

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