Endogenous Phospholipid Metabolite Containing Topical Product Inhibits Ultraviolet Light-Induced Inflammation and DNA Damage in Human Skin

Background: N-palmitoylethanolamine (PEA) and organic osmolytes are endogenous components of the human epidermis and are generated from phospholipids in the stratum granulosum. PEA has been shown to exert potent antioxidant and anti-inflammatory activities. The endogenous organic osmolytes such as b...

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Veröffentlicht in:Skin pharmacology and physiology 2007-01, Vol.20 (3), p.155-161
Hauptverfasser: Kemeny, L., Koreck, A., Kis, K., Kenderessy-Szabo, A., Bodai, L., Cimpean, A., Paunescu, V., Raica, M., Ghyczy, M.
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Sprache:eng
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Zusammenfassung:Background: N-palmitoylethanolamine (PEA) and organic osmolytes are endogenous components of the human epidermis and are generated from phospholipids in the stratum granulosum. PEA has been shown to exert potent antioxidant and anti-inflammatory activities. The endogenous organic osmolytes such as betaine and sarcosine control skin humidity, but have also been shown to inhibit ultraviolet (UV) light-induced oxidative stress in keratinocytes. Objectives: To investigate the effect of a PEA- and organic osmolyte-containing topical product (Physiogel AI®) on the development of UV light-induced erythema, thymine dimer formation and p53 tumor suppressor gene activation, as well as intercellular adhesion molecule 1 (ICAM-1) and Ki67 expression in normal human skin. Methods: The UV-induced erythema was measured by a spectrofluorometric method. Thymine dimers, p53, ICAM-1 and Ki67 were detected in skin biopsies using immunohistochemistry. Results: Physiogel AI cream significantly inhibited the development of UV light-induced erythema and thymine dimer formation in normal human skin, but did not alter the number of Ki67+ proliferating keratinocytes and the expression of p53 and ICAM-1. Conclusions: Our results suggest that PEA and organic osmolytes might represent a new generation of compounds which suppress UV-induced photodamage.
ISSN:1660-5527
1660-5535
DOI:10.1159/000098702