Received for review December 21, 2006. Revised manuscript received June 18, 2007. Accepted June 21, 2007. This research was made possible by Grant P01 ES012020 from the National Institute of Environmental Health Sciences (NIEHS) and the Office of Dietary Supplements (ODS), NIH, and by Grant 95P50AT004155 from the National Center of Complementary and Alternative Medicine (NCCAM) and ODS, NIH. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the ODS, NIEHS, NCCAM, or NIH.

Abstract:

Inhibition of prostaglandin E₂ (PGE₂) production in lipopolysaccharide-stimulated RAW264.7 mouse macrophage cells was assessed with an enzyme immunoassay following treatments with Echinacea extracts or synthesized alkamides. Results indicated that ethanol extracts diluted in media to a concentration of 15 g/mL from E. angustifolia, E. pallida, E. simulata, and E. sanguinea significantly inhibited PGE₂ production. In further studies, PGE₂ production was significantly reduced by all synthesized alkamides assayed at 50 M, by Bauer alkamides 8, 12A analogue, and 14, Chen alkamide 2, and Chen alkamide 2 analogue at 25 M and by Bauer alkamide 14 at 10 M. Cytotoxicity did not play a role in the noted reduction of PGE₂ production in either the Echinacea extracts or synthesized alkamides. High-performance liquid chromatography analysis identified individual alkamides present at concentrations below 2.8 M in the extracts from the six Echinacea species (15 g/mL crude extract). Because active extracts contained <2.8 M of specific alkamide and the results showed that synthetic alkamides must have a minimum concentration of 10 M to inhibit PGE₂, it is likely that alkamides may contribute toward the anti-inflammatory activity of Echinacea in a synergistic or additive manner.

Keywords: Echinacea purpurea; Echinacea angustifolia; Echinacea pallida; Echinacea tennesseensis; Echinacea simulata; Echinacea sanguinea; anti-inflammatory; cytotoxicity

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