Plant polyphenols effectively protect HaCaT cells from ultraviolet C-triggered necrosis and suppress inflammatory chemokine expression.
Oxidative stress is a common response of epidermal cells to a variety of noxious stimuli such as ultraviolet (UV) radiation from solar light and proinflammatory cytokines from skin-infiltrating leukocytes. Here, we report that two types of plant-derived antioxidants, the phenylpropanoid glycoside verbascoside as well as the flavonoids rutin and quercetin possess protective effects against UVC-induced cell damage and proinflammatory activation. The molecules under investigation were effective against the loss of cell integrity associated with necrosis in doses consistent with their antioxidant activity, whereas they did not significantly oppose UVC-induced proliferation arrest and apoptosis. By contrast, only verbascoside effectively inhibited cytokine-induced release of proinflammatory mediators in a dose-dependent fashion. Verbascoside and its homologue teupolioside dramatically impaired NF-kappaB and AP-1 DNA binding activity. These results suggest that plant polyphenols with antioxidant properties have distinct mechanisms in the suppression of oxidative stress induced in keratinocytes by different stimuli. Verbascoside and teupolioside are hence of potential interest in the protection of the skin from both environmental and inflammatory insults.
Pastore
Saveria
S
Laboratory of Tissue Engineering and Cutaneous Physiopathology, Istituto Dermopatico dell'Immacolata, IRCCS, Rome, Italy. pastore@idi.it
Potapovich
Alla
A
Kostyuk
Vladimir
V
Mariani
Valentina
V
Lulli
Daniela
D
De Luca
Chiara
C
Korkina
Liudmila
L
D031328:Ajuga / Q000737:chemistry; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000528:radiation effects; D015153:Blotting, Western; D002460:Cell Line; D018925:Chemokines / Q000378:metabolism*; D004247:DNA / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005960:Glucosides / Q000494:pharmacology*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007371:Interferon-gamma / Q000494:pharmacology; D015603:Keratinocytes / Q000187:drug effects* / Q000378:metabolism / Q000528:radiation effects; D016328:NF-kappa B / Q000378:metabolism; D009336:Necrosis; D010636:Phenols / Q000494:pharmacology*; D010766:Phosphorylation / Q000187:drug effects; D010936:Plant Extracts / Q000737:chemistry / Q000494:pharmacology*; D011485:Protein Binding / Q000187:drug effects; D011794:Quercetin / Q000494:pharmacology; D012431:Rutin / Q000494:pharmacology; D031662:Syringa / Q000737:chemistry; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D014466:Ultraviolet Rays; D059808:Polyphenols
D000975:Antioxidants; D018925:Chemokines; D004247:DNA; D048049:Extracellular Signal-Regulated MAP Kinases; D005960:Glucosides; D018836:Inflammation Mediators; D007371:Interferon-gamma; D016328:NF-kappa B; D010636:Phenols; D010936:Plant Extracts; D011794:Quercetin; D012431:Rutin; D018808:Transcription Factor AP-1; D014409:Tumor Necrosis Factor-alpha; C058956:acteoside; D059808:Polyphenols