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

• Published in: Mediators of inflammation Vol. 2021; p. 9330596
• Main Authors: 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, Jr, Waldiceu A, Casagrande, Rúbia
• Format: Journal Article
• Language: English
• Published: United States 2021
• Subjects: Administration, Topical; Animals; Mice; Mice, Hairless; Oxidative Stress; Prostaglandins - metabolism; Skin - metabolism; Ultraviolet Rays
• ISSN: 1466-1861

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- -prostaglandin J (15d-PGJ ) 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 (30, 90, and 300 ng/mouse) (TFcPGJ ) in the skin of hairless mice. UVB increased skin edema, myeloperoxidase activity, metalloproteinase-9 activity, lipid peroxidation, superoxide anion production, gp91 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 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 indicates it is a promising therapeutic approach against cutaneous inflammatory and oxidative pathological alterations.