Lipoxin A4 inhibits UV radiation-induced skin inflammation and oxidative stress in mice

Martínez, Renata M.; Fattori, Victor; Saito, Priscila; Melo, C.B.P.; Borghi, Sérgio M.; Pinto, Ingrid C.; Bussmann, Allan J. C.; Baracat, Marcela M.; Georgetti, Sandra R.; Verri, Waldiceu A.; Casagrande, Rúbia

doi:10.1016/j.jdermsci.2018.04.014

Cited by 41 publications

(69 citation statements)

References 62 publications

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“…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 ). Recently, 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 ). However, there was no evidence on the therapeutic effect of a pro-resolving lipid mediators derived from DHA metabolism on UVB skin inflammation and oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2018

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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.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2018

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“…Exposure to UVB radiation leads to an increase in the production of pro-inflammatory and anti-inflammatory cytokines [16,[27][28][29]. Therefore, we subsequently aimed to determine whether BML-111 could affect UVB-induced cytokine production.…”

Section: Bml-111 Reduces Cytokine Production During Uvb-induced Skin mentioning

confidence: 99%

“…ALX/FPR2 is widely expressed throughout the organs such as skin and gastrointestinal tract and in immune cells, including neutrophils, monocytes, mast cells, and macrophages [14,15]. Specifically for skin inflammation induced by UVB, treatment with LXA4 [16], MaR1 [17], and RvD1 [18] ameliorate the signs of skin inflammation, indicating that this class of molecules can actively treat UVB-induced inflammation. Given that SPMs can be chemically unstable and often inactivated within tissues near the site of formation [19], stable analogs are required.…”

Section: Introductionmentioning

confidence: 99%

The Lipoxin Receptor/FPR2 Agonist BML-111 Protects Mouse Skin Against Ultraviolet B Radiation

et al. 2020

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Excessive exposure to UV, especially UVB, is the most important risk factor for skin cancer and premature skin aging. The identification of the specialized pro-resolving lipid mediators (SPMs) challenged the preexisting paradigm of how inflammation ends. Rather than a passive process, the resolution of inflammation relies on the active production of SPMs, such as Lipoxins (Lx), Maresins, protectins, and Resolvins. LXA4 is an SPM that exerts its action through ALX/FPR2 receptor. Stable ALX/FPR2 agonists are required because SPMs can be quickly metabolized within tissues near the site of formation. BML-111 is a commercially available synthetic ALX/FPR2 receptor agonist with analgesic, antioxidant, and anti-inflammatory properties. Based on that, we aimed to determine the effect of BML-111 in a model of UVB-induced skin inflammation in hairless mice. We demonstrated that BML-111 ameliorates the signs of UVB-induced skin inflammation by reducing neutrophil recruitment and mast cell activation. Reduction of these cells by BML-111 led to lower number of sunburn cells formation, decrease in epidermal thickness, collagen degradation, cytokine production (TNF-α, IL-1β, IL-6, TGF, and IL-10), and oxidative stress (observed by an increase in total antioxidant capacity and Nrf2 signaling pathway), indicating that BML-111 might be a promising drug to treat skin disorders.

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“…Skin‐associated cells produce inflammatory cytokines such as TNF‐α and IL‐1β that play important roles in UV‐induced skin injury, due to their action of inducing sunburn cells development, leucocyte recruitment and ROS‐generating systems . Therefore, we investigated whether EcPDTC could repress skin inflammation by targeting cytokine production.…”

Section: Resultsmentioning

confidence: 99%

“…Skin-associated cells produce inflammatory cytokines such as TNF-a and IL-1b that play important roles in UVinduced skin injury, due to their action of inducing sunburn cells development, leucocyte recruitment and ROSgenerating systems. [52,57,58] Therefore, we investigated whether EcPDTC could repress skin inflammation by targeting cytokine production. UVB irradiation stimulated the production of the pro-inflammatory cytokines TNF-a (Figure 9a) and IL-1b (Figure 9b) compared to non-irradiated mice.…”

Section: Ecpdtc Inhibits Uvb Irradiation-induced Cytokine Productionmentioning

confidence: 99%

Topical emulsion containing pyrrolidine dithiocarbamate: effectiveness against ultraviolet B irradiation-induced injury of hairless mouse skin

Martínez

Ivan

Vale

et al. 2018

Journal of Pharmacy and Pharmacology

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Lipoxin A4 inhibits UV radiation-induced skin inflammation and oxidative stress in mice

Abstract: LXA inhibited UV radiation-induced skin inflammation by diminishing pro-inflammatory cytokine production and oxidative stress as well as inducing anti-inflammatory cytokines and Nrf2.

Cited by 41 publications

References 62 publications

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

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

The Lipoxin Receptor/FPR2 Agonist BML-111 Protects Mouse Skin Against Ultraviolet B Radiation

Topical emulsion containing pyrrolidine dithiocarbamate: effectiveness against ultraviolet B irradiation-induced injury of hairless mouse skin

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