Biol. Pharm. Bull., 28(4),601-606, April 2005

Regular Articles

Avena Rhealba® Inhibits A23187-Stimulated Arachidonic Acid Mobilization, Eicosanoid Release, and cPLA2 Expression in Human Keratinocytes: Potential in Cutaneous Inflammatory Disorders


Marie-Françoise ARIES,*,a Clémence VAISSIERE,a Eric PINELLI,b Bernard PIPY,c and Marie CHARVERONa

a CERPER, Institut de Recherche Pierre Fabre, Laboratoire de Biologie Cellulaire Cutanée; BP 3071, 2 rue Viguerie, 31025 Toulouse Cédex 3, France: b Ecole Nationale Supérieure Agronomique de Toulouse; 1 avenue de l'Agrobiopˆole, Auzeville Tolosane, BP 107 F, 31326 Castanet Tolosan Cedex, France: and c UPRES EA2405, INSERM IFR31, CHU Rangueil; 1 avenue Jean Poulhes, 31403 Toulouse Cedex 4, France. * To whom correspondence should be addressed. e-mail: marie.francoise.aries@pierre-fabre.com

The aim of the present study was to examine the effects of Avena Rhealba® (AR) oatmeal extract on the metabolism of arachidonic acid (AA) and eicosanoids as well as on the expression of cytosolic phospholipase A2 (cPLA2) in the human keratinocyte cell line HaCaT. For this purpose, we examined the effects of AR on basal and A23187-triggered release of [3H]-AA from phospholipids and on the production of [3H]-labeled metabolites of the cyclooxygenase (CO) and 5-lipoxygenase (LO) pathways. AR was found to inhibit A23187-triggered [3H]-AA mobilization from phospholipids (p<0.05) and production of [3H]-labeled metabolites of CO (p<0.05) and LO (p<0.05) pathways. These results suggest AR decreases PLA2-dependent mobilization of AA from phospholipids. A closer examination of the effects of AR on prostaglandin 6KF1α (6KPGF1α), the stable metabolite of prostacyclin, revealed dose-dependent inhibition of this AA metabolite. AR also decreased A23187- and tumor necrosis factor α-induced cPLA2 overexpression, as shown by cPLA2 immunodetection and mRNA expression. These results demonstrate the high potential of AR in the treatment of inflammatory diseases of the skin.

Key words Avena Rhealba®; keratinocyte; arachidonic acid; eicosanoid; cytosolic phospholipase A2