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Topical Administration of 15-Deoxy-Δ(12,14)-Prostaglandin J(2) Using a Nonionic Cream: Effect on UVB-Induced Skin Oxidative, Inflammatory, and Histopathological Modifications in Mice

UVB radiation is certainly one of the most important environmental threats to which we are subjected to. This fact highlights the crucial protective role of the skin. However, the skin itself may not be capable of protecting against UVB depending on irradiation intensity and time of exposition. Sun...

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Detalles Bibliográficos
Autores principales: Kumagai, Clovis M., Martinez, Renata M., Colombo, Barbara B., Saito, Priscila, Pinto, Ingrid C., Rodrigues, Camilla C. A., Vale, David L., Matos, Ricardo L. N., Bracarense, Ana P. F. R. L., Baracat, Marcela M., Georgetti, Sandra R., Clemente-Napimoga, Juliana T., Napimoga, Marcelo H., Fattori, Victor, Verri, Waldiceu A., Casagrande, Rúbia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8577928/
https://www.ncbi.nlm.nih.gov/pubmed/34764817
http://dx.doi.org/10.1155/2021/9330596
Descripción
Sumario:UVB radiation is certainly one of the most important environmental threats to which we are subjected to. This fact highlights the crucial protective role of the skin. However, the skin itself may not be capable of protecting against UVB depending on irradiation intensity and time of exposition. Sun blockers are used to protect our skin, but they fail to fully protect it against oxidative and inflammatory injuries initiated by UVB. To solve this issue, topical administration of active molecules is an option. 15-Deoxy-Δ(12,14)-prostaglandin J(2) (15d-PGJ(2)) is an arachidonic acid-derived lipid with proresolution and anti-inflammatory actions. However, as far as we are aware, there is no evidence of its therapeutic use in a topical formulation to treat the deleterious events initiated by UVB, which was the aim of the present study. We used a nonionic cream to vehiculate 15d-PGJ(2) (30, 90, and 300 ng/mouse) (TFcPGJ(2)) in the skin of hairless mice. UVB increased skin edema, myeloperoxidase activity, metalloproteinase-9 activity, lipid peroxidation, superoxide anion production, gp91(phox) and COX-2 mRNA expression, cytokine production, sunburn and mast cells, thickening of the epidermis, and collagen degradation. UVB also diminished skin ability to reduce iron and scavenge free radicals, reduced glutathione (GSH), sulfhydryl proteins, and catalase activity. TFcPGJ(2) inhibited all these pathological alterations in the skin caused by UVB. No activity was observed with the unloaded topical formulation. The protective outcome of TFcPGJ(2) indicates it is a promising therapeutic approach against cutaneous inflammatory and oxidative pathological alterations.