The Lipid Mediator Resolvin D1 Reduces the Skin Inflammation and Oxidative Stress Induced by UV Irradiation in Hairless Mice

UV irradiation-induced oxidative stress and inflammation contribute to the development of skin diseases. Therefore, targeting oxidative stress and inflammation might contribute to reduce skin diseases. Resolvin D1 (RvD1) is a bioactive metabolite generated during inflammation to actively orchestrate...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in pharmacology Vol. 9; p. 1242
Main Authors Saito, Priscila, Melo, Cristina P B, Martinez, Renata M, Fattori, Victor, Cezar, Talita L C, Pinto, Ingrid C, Bussmann, Allan J C, Vignoli, Josiane A, Georgetti, Sandra R, Baracat, Marcela M, Verri, Jr, Waldiceu A, Casagrande, Rubia
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 31.10.2018
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:UV irradiation-induced oxidative stress and inflammation contribute to the development of skin diseases. Therefore, targeting oxidative stress and inflammation might contribute to reduce skin diseases. Resolvin D1 (RvD1) is a bioactive metabolite generated during inflammation to actively orchestrate the resolution of inflammation. However, the therapeutic potential of RvD1 in UVB skin inflammation remains undetermined, which was, therefore, the aim of the present study. The intraperitoneal treatment with RvD1 (3-100 ng/mouse) reduced UVB irradiation-induced skin edema, myeloperoxidase activity, matrix metalloproteinase 9 activity, and reduced glutathione depletion with consistent effects observed with the dose of 30 ng/mouse, which was selected to the following experiments. RvD1 inhibited UVB reduction of catalase activity, and hydroperoxide formation, superoxide anion production, and gp91phox mRNA expression. RvD1 also increased the Nrf2 and its downstream targets NQO1 and HO-1 mRNA expression. Regarding cytokines, RvD1 inhibited UVB-induced production of IL-1β, IL-6, IL-33, TNF-α, TGF-β, and IL-10. These immuno-biochemical alterations by RvD1 treatment had as consequence the reduction of UVB-induced epidermal thickness, sunburn and mast cell counts, and collagen degradation. Therefore, RvD1 inhibited UVB-induced skin oxidative stress and inflammation, rendering this resolving lipid mediator as a promising therapeutic agent.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Edited by: Mauro Perretti, Queen Mary University of London, United Kingdom
Reviewed by: Antonio Recchiuti, Università degli Studi G. d'Annunzio Chieti e Pescara, Italy; Emanuela Marcantoni, New York University, United States
Waldiceu A. Verri Jr. orcid.org/0000-0003-2756-9283
This article was submitted to Inflammation Pharmacology, a section of the journal Frontiers in Pharmacology
ISSN:1663-9812
1663-9812
DOI:10.3389/fphar.2018.01242