Topical Administration of 15-Deoxy-Δ12,14-Prostaglandin J2 Using a Nonionic Cream: Effect on UVB-Induced Skin Oxidative, Inflammatory, and Histopathological Modifications in Mice
Autor: | Waldiceu A. Verri, Renata M. Martinez, A.P.F.R.L. Bracarense, Marcelo Henrique Napimoga, Priscila Saito, Rubia Casagrande, Victor Fattori, Sandra R. Georgetti, Camilla C. A. Rodrigues, David L. Vale, Clovis M. Kumagai, Marcela M. Baracat, Barbara B. Colombo, Ricardo Luís Nascimento de Matos, Juliana Trindade Clemente-Napimoga, Ingrid C. Pinto |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Article Subject
Ultraviolet Rays medicine.medical_treatment Administration Topical Immunology Pharmacology Lipid peroxidation chemistry.chemical_compound Mice medicine Pathology Animals RB1-214 Sunburn skin and connective tissue diseases Skin Mice Hairless biology Epidermis (botany) integumentary system Chemistry Superoxide Cell Biology Glutathione medicine.disease Hairless Oxidative Stress Cytokine Catalase biology.protein Prostaglandins Research Article |
Zdroj: | Mediators of Inflammation, Vol 2021 (2021) Mediators of Inflammation |
ISSN: | 1466-1861 |
Popis: | 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-Δ12,14-prostaglandin J2 (15d-PGJ2) 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-PGJ2 (30, 90, and 300 ng/mouse) (TFcPGJ2) in the skin of hairless mice. UVB increased skin edema, myeloperoxidase activity, metalloproteinase-9 activity, lipid peroxidation, superoxide anion production, gp91phox 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. TFcPGJ2 inhibited all these pathological alterations in the skin caused by UVB. No activity was observed with the unloaded topical formulation. The protective outcome of TFcPGJ2 indicates it is a promising therapeutic approach against cutaneous inflammatory and oxidative pathological alterations. |
Databáze: | OpenAIRE |
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