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Vasoprotective and anti-inflammatory ingredient for Rosacea: in vitro assessment


Author: Samara Eberlin

Published at: October 08, 2014

23rd EADV Congress (European Academy of Dermatology and Venereology); Amsterdam, October 8-12, 2014.
Costa A, Eberlin S, Polettini AJ, Jorge ACF, Eberlin S, Pereira AFC, Cascais LC, Dolis E, Frazilho M, Lage R, Torloni LBO.


Rosacea is a chronic inflammatory dermatosis characterized by flushing, permanent erythema, telangiectasia, papules, and pustules on the central area of the face, affecting middle-aged patients. Its underlying pathophysiological mechanisms are not completely understood, although the disturbances observed are related to vascular reactivity and inflammatory response. Local production of inflammatory mediators, such as prostaglandins (PG) and histamine (HI), leads to vasodilation and increased vascular permeability due to additional release of VEGF (vascular endothelial growth factor) and inducible nitric oxide synthase (iNOS). In this study, we evaluated the effects of an active ingredient (AI) on the production of PGE2, HI, VEGF, and iNOS, using an in vitro model of human keratinocytes. Incubation of cell cultures with IL-1β promoted significant increases in the synthesis of HI, PGE2, VEGF, and iNOS compared to the control group. Concomitant treatment of cell cultures with AI prevented the increase of all evaluated mediators. In relation to HI and PGE2, AI was able to reduce the levels by up to 24.8% and 47%, respectively, compared to the IL-1β-stressed group. Increased levels of VEGF and iNOS were also prevented, reaching 51.2% and 100%, respectively, in relation to the IL-1β-stressed group. Flushing is one of the most evident signs in Rosacea, and increased blood flow in the superficial dermis is the main factor responsible for this phenomenon. In this work, it was demonstrated that AI exerts vasoprotective and anti-inflammatory effects, suggesting a possible application in skin care product formulations to contribute to the amelioration of Rosacea symptoms.