Inicio  /  Antioxidants  /  Vol: 8 Par: 5 (2019)  /  Artículo
ARTÍCULO
TITULO

Vitis vinifera L. Leaf Extract Inhibits In Vitro Mediators of Inflammation and Oxidative Stress Involved in Inflammatory-Based Skin Diseases

Enrico Sangiovanni    
Chiara Di Lorenzo    
Stefano Piazza    
Yuri Manzoni    
Cecilia Brunelli    
Marco Fumagalli    
Andrea Magnavacca    
Giulia Martinelli    
Francesca Colombo    
Antonella Casiraghi    
Gloria Melzi    
Laura Marabini    
Patrizia Restani and Mario Dell?Agli    

Resumen

Psoriasis is a chronic cutaneous condition characterized by the release of pro-inflammatory mediators and oxidative stress. The reduction of these factors is currently the most effective strategy to inhibit the symptoms of pathology. Antioxidants from natural sources are increasingly used to improve skin conditions. Dried red leaves from grapevine (Vitis vinifera L., cv Teinturiers) showed anti-inflammatory and anti-bacterial activities, but their possible effects on keratinocytes have not been previously investigated. In this study we tested the ability of a water extract from grapevine leaves (VVWE) to inhibit inflammatory conditions in human keratinocytes (HaCaT cells), challenged with proinflammatory (tumor necrosis factor-a (TNF-a) or lipopolysaccharide (LPS)) or prooxidant (ultraviolet B radiation (UVB) or H2O2) mediators. VVWE inhibited interleukin-8 (IL-8) secretion induced by proinflammatory stimuli, acting on the IL-8 promoter activity, but the effect was lower when prooxidant mediators were used. The effect was partly explained by the reduction of nuclear factor-?B (NF-?B)-driven transcription and nuclear translocation. Furthermore, vascular endothelial growth factor (VEGF) secretion, a regulator of angiogenesis, was inhibited by VVWE, but not matrix metalloproteinase-9 (MMP-9), a protease involved in matrix remodeling. VVWE, assayed on Franz diffusion cell system, showed a marked reduction of High Performance Liquid Chromatography (HPLC)-identified compounds. Pure molecules individually failed to reduce TNF-a-induced IL-8 release, suggesting synergistic effects or the presence of other bioactive compounds still unknown.

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