Aspirin-Triggered Resolvin D1 (AT-RvD1) Protects Mouse Skin against UVB-Induced Inflammation and Oxidative Stress

• Published in: Molecules (Basel, Switzerland) Vol. 28; no. 5; p. 2417
• Main Authors: Melo, Cristina P B, Saito, Priscila, Martinez, Renata M, Staurengo-Ferrari, Larissa, Pinto, Ingrid C, Rodrigues, Camilla C A, Badaro-Garcia, Stephanie, Vignoli, Josiane A, Baracat, Marcela M, Bussmann, Allan J C, Georgetti, Sandra R, Verri, Waldiceu A, Casagrande, Rubia
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.03.2023; MDPI
• Subjects: 17(R)RvD1; Animals; Anti-inflammatory agents; Antioxidants; Antioxidants - pharmacology; Arthritis; Aspirin; Aspirin - pharmacology; Catalase; ciclooxygenase-2; Collagen; Cytokines; Docosahexaenoic Acids - pharmacology; Edema; Enzymes; Exposure; Gelatinase B; Gene expression; Hairless; Inflammation; Leukocytes (neutrophilic); lipid mediator; Lipids; Mice; Neutrophils; NF-E2-Related Factor 2 - metabolism; Nrf2; Oxidative Stress; Radiation; ROS; Skin; Sunburn; Ultraviolet radiation; Ultraviolet Rays; ciclooxygenase-2; ultraviolet radiation; 17(R)RvD1; neutrophil infiltration; Nrf2; antioxidant capacity; ROS; lipid mediator; cytokines; sunburn
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules28052417

Intense exposure to UVB radiation incites excessive production of reactive oxygen species (ROS) and inflammation. The resolution of inflammation is an active process orchestrated by a family of lipid molecules that includes AT-RvD1, a specialized proresolving lipid mediator (SPM). AT-RvD1 is derived from omega-3, which presents anti-inflammatory activity and reduces oxidative stress markers. The present work aims to investigate the protective effect of AT-RvD1 on UVB-induced inflammation and oxidative stress in hairless mice. Animals were first treated with 30, 100, and 300 pg/animal AT-RvD1 (i.v.) and then exposed to UVB (4.14 J/cm ). The results showed that 300 pg/animal of AT-RvD1 could restrict skin edema, neutrophil and mast cell infiltration, COX-2 mRNA expression, cytokine release, and MMP-9 activity and restore skin antioxidant capacity as per FRAP and ABTS assays and control O production, lipoperoxidation, epidermal thickening, and sunburn cells development. AT-RvD1 could reverse the UVB-induced downregulation of Nrf2 and its downstream targets GSH, catalase, and NOQ-1. Our results suggest that by upregulating the Nrf2 pathway, AT-RvD1 promotes the expression of ARE genes, restoring the skin's natural antioxidant defense against UVB exposition to avoid oxidative stress, inflammation, and tissue damage.