Abstract
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.
Highlights
The skin is the largest organ of the human body and the main protection barrier of the organism against chemical, physical, and biological aggressors (Afaq et al, 2005; Fonseca et al, 2011; Khavkin and Ellis, 2011)
reactive oxygen species (ROS) are directly involved in the induction of the inflammatory process and oxidative stress, because they stimulate the secretion of cytokines (Ivan et al, 2014) and the depletion of endogenous antioxidants (Zaid et al, 2007; Halliwell, 2009)
We demonstrated for the first time that lipoxin A4, a pro-resolution lipid mediator derived from the arachidonic acid, reduces UVB irradiation-induced skin inflammation and oxidative stress (Martinez et al, 2018)
Summary
The skin is the largest organ of the human body and the main protection barrier of the organism against chemical, physical, and biological aggressors (Afaq et al, 2005; Fonseca et al, 2011; Khavkin and Ellis, 2011). External aggressors include exposure to UV irradiation, the main cause of skin damage. Considering the synergistic effect of the production of ROS and inflammatory mediators, the improvement of the endogenous antioxidant system and the resolution of inflammation become promising approaches to prevent and treat UVB irradiation-induced skin damage (Fonseca et al, 2010; Serhan, 2014)
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