Epidermal anti-Inflammatory properties of 5,11,14 20:3: Effects on mouse ear edema, PGE2 levels in cultured keratinocytes, and PPAR activation

doi:10.1186/1476-511X-1-5

Lipids in Health and Disease

Volume 1

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Berger A
Monnard I
Baur M
Charbonnet C
Safonova I
Jomard A

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Monnard I
Baur M
Charbonnet C
Safonova I
Jomard A
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Research

Epidermal anti-Inflammatory properties of 5,11,14 20:3: Effects on mouse ear edema, PGE₂levels in cultured keratinocytes, and PPAR activation

Alvin Berger¹^,3 , Irina Monnard¹ , Markus Baur¹^,4 , Corinne Charbonnet¹^,5 , Irina Safonova² and André Jomard²

¹Nestlé Research Center, Vers-Chez-les-Blanc, 1000 Lausanne 26, Switzerland

²Galderma R&D, Route des Lucioles, BP 87, 06902 Sophia Antipolis, France

³Current address: Cytochroma, Inc., Manager Lipidomics™, 330 Cochrane Drive, Markham, Ontario L3R 8E4, Canada

⁴Current address: Boehringer Ingelheim Pharma KG, Biopharmaceutical Quality & Development, Head of Manufacturing Alliances, Birkendorfer Str. 65, 88397 Biberach / Riss, Germany

⁵Current address: chemin de Vuichardaz 9, CH-1030 Bussigny-près-Lausanne, Switzerland

author email corresponding author email

Lipids in Health and Disease 2002, 1:5doi:10.1186/1476-511X-1-5


Published:	6 December 2002

Abstract

Background

5,11,14 20:3 is similar to 20:4n-6 but lacks the internal Δ8 double bond essential for prostaglandin and eicosanoid synthesis. When previously fed to laboratory animals as a gymnosperm seed oil component it has shown anti-inflammatory properties.

Results

Herein, topically applied Podocarpus nagi methyl esters (containing 26% 5,11,14 20:3) were incorporated into mouse ear phospholipids, reduced 20:4n-6, and reduced 20:4n-6- and TPA-induced mouse ear edema. Purified 5,11,14 20:3 was taken up by cultured human skin keratinocytes, reduced 20:4n-6, and reduced PGE₂levels dramatically. Purified 5,11,14 20:3 did not affect PPARα, PPARγ, or PPARδ transactivation.

Conclusions

Topical application of 5,11,14 20:3 to skin surfaces can thus reduce inflammatory processes, most likely by displacing 20:4n-6 from phospholipid pools and reducing downstream inflammatory products derived from 20:4n-6 such as PGE₂and leukotrienes. It could have potential use in treating clinical skin disorders resulting from overproduction of 20:4n-6-derived eicosanoid products.