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Int Immunopharmacol. 2009 Oct;9(11):1260-4. doi: 10.1016/j.intimp.2009.08.009. Epub 2009 Aug 25.

Role for PPARgamma in IL-2 inhibition in T cells by Echinacea-derived undeca-2E-ene-8,10-diynoic acid isobutylamide.

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1
University of North Carolina Greensboro, Department of Chemistry and Biochemistry, P.O. Box 26170, Greensboro, NC 27405, USA.

Abstract

Certain fatty acid amides from Echinacea spp. have demonstrated moderate to high cannabinoid activity. As a result, CB2 activation is currently hypothesized to be the basis of activity for immunomodulation by Echinacea spp. PPARgamma, an orphan nuclear receptor and lipid sensor, is known to inhibit IL-2 production and be activated by fatty acid derivatives such as the endocannabinoids. In these investigations, we demonstrate that undeca-2E-ene-8,10-diynoic acid, an Echinacea angustifolia-derived alkylamide lacking affinity for the CB2 receptor, inhibits IL-2 secretion in Jurkat T cells through PPARgamma activity at low micromolar concentrations (330 ng/mL). The IL-2 inhibition is reversed by the addition of the selective PPARgamma antagonist T0070907. Additionally, we show that that undeca-2-ene-8,10-diynoic acid stimulates 3T3-L1 differentiation, a process dependent on PPARgamma activity. These experiments demonstrate that PPARgamma is involved in T cell IL-2 inhibition by undeca-2-ene-8,10-diynoic acid and suggest that cytokine modulation by the alkylamides is due to polyvalent activity.

PMID:
19712756
DOI:
10.1016/j.intimp.2009.08.009
[Indexed for MEDLINE]
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