10-Hydroxy-2-decenoic acid, a natural fatty acid only found in royal jelly, may be of value in correcting skin barrier dysfunction. We evaluated the activity of Hydroxydecine^[2], its synthetic counterpart, in vitro on the regulation of epidermal differentiation markers, ex vivo on the inflammatory response and restoration of skin barrier function, and in vivo on UV-induced xerosis in healthy human volunteers.

In cultured normal human keratinocytes, Hydroxydecine induced involucrin, transglutaminase-1 and filaggrin protein production. In topically Hydroxydecine-treated skin equivalents, immunohistochemical analysis revealed an increase in involucrin, transglutaminase-1 and filaggrin staining.

In a model of thymic stromal lymphopoietin (TSLP)-induced inflamed epidermis, a Hydroxydecine-containing emulsion inhibited TSLP release. In a model of inflammation and barrier impairment involving human skin explants maintained alive, Hydroxydecine balm restored stratum corneum cohesion and significantly increased filaggrin expression, as shown by immunohistochemistry. It also decreased pro-inflammatory cytokine secretion (IL-4, IL-5 and IL-13).

In healthy volunteers with UV-induced xerosis, the hydration index increased by +28.8% and +60.4% after 7 and 21 days of treatment with Hydroxydecine cream, respectively.

Hydroxydecine thus proved its efficacy in activating keratinocyte differentiation processes in vitro, restoring skin barrier function and reducing inflammation ex vivo, and hydrating dry skin in vivo.

References

1. ^{^} Eur J Dermatol (www.jle.com)
2. ^{^} Hydroxydecine (www.beaute-test.com)