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United States Department of Agriculture

Agricultural Research Service

Title: Methyl ester of avenathramide-C inhibits tumor necrosis factor-alpha (TNF-alpha) and interlenkin-Ibeta(IL-beta)-induced NF-kappaB activation in endothelial cells

Authors
item Guo, Weimin - TUFTS/HNRCA
item Wise, Mitchell
item Peterson, David
item Meydani, Mohsen

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: April 1, 2006
Publication Date: April 1, 2006
Citation: Guo, W., Wise, M.L., Peterson, D., Meydani. 2006. Methyl ester of avenanthramide-c inhibits tnfalpha- and il-1beta-induced nf-kappab activation in endothelial cells. Federation of American Societies for Experimental Biology Conference. 20:A1000.

Technical Abstract: Atherosclerosis is a chronic inflammatory disease accompanied by the expression of endothelial proinflammatory molecules. Avenanthramides (Avn) are polyphenols which are present exclusively in oats. We have reported the avenanthramide-enriched mixture extracted from oats significantly suppressed interleukin (IL)-1beta-stimulated secretion of proinflammatory cytokines IL-6, IL-8 and monocyte chemoattractant protein (MCP)-1 in human aortic endothelial cell (HAEC). Here we report that these effects could be mediated by Avn interference with the nuclear factor kappaB (NF-kappaB) dependent transcription. We used synthetically prepared methyl ester of Avn-c (CH3-Avn-c), which shows a higher potency than non-methylated form, to examine its effect on IL-1b- and TNFalpha-stimulated NF-kappaB activation as assessed with NF-kappaB DNA binding assay as well as NF-kappaB luciferase reporter assay. CH3-Avn-c significantly and dose-dependently decreased IL-6, IL-8 and MCP-1 secretion in human vascular endothelial cells as determined by ELISA and inhibited IL-1beta- and TNFalpha-stimulated NF-kB activation as determined in NF-kappaB DNA binding assay and NF-kappaB luciferase reporter assay. However, the proteasome activity was only mildly inhibited by CH3-Avn-c. These results suggest that the CH3-Avn-c decreased expression of endothelial proinflammatory cytokines at least partially through inhibiting NF-kappaB activation, likely by inhibiting an upstream signaling component.

Last Modified: 12/25/2014