Abstract
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-Δ12,14-prostaglandin J2 (15d-PGJ2) 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-PGJ2 (30, 90, and 300 ng/mouse) (TFcPGJ2) in the skin of hairless mice. UVB increased skin edema, myeloperoxidase activity, metalloproteinase-9 activity, lipid peroxidation, superoxide anion production, gp91phox 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. TFcPGJ2 inhibited all these pathological alterations in the skin caused by UVB. No activity was observed with the unloaded topical formulation. The protective outcome of TFcPGJ2 indicates it is a promising therapeutic approach against cutaneous inflammatory and oxidative pathological alterations.
Highlights
15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) is a cyclopentenone prostaglandin formed upon the spontaneous dehydration of prostaglandin D2 into 15d-PGJ2 [1]
Topical Formulation Containing 15d-PGJ2 (TFcPGJ2) Reduced the Skin Edema, MPO Activity, and MMP-9 Activity/Secretion Increase Caused by UVB Irradiation
The first set of experiments evaluated whether topical formulation containing 15d-PGJ2 (TFcPGJ2) would inhibit skin inflammation in a dose-dependent manner (30, 90, and 300 ng/animal) having UVB irradiation as the stimulus (Figure 2)
Summary
15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) is a cyclopentenone prostaglandin formed upon the spontaneous dehydration of prostaglandin D2 into 15d-PGJ2 [1]. The literature mentioned above makes clear that there is still controversy whether 15d-PGJ2 is a treatment or aggravates atopic dermatitis, which is an inflammatory skin disease This is obviously a difficult question to answer, which is related to the varied experimental conditions that each study used in terms of the route of administration, dose/concentration, disease model, and timeframe of disease in which 15dPGJ2 was administrated. Despite these data, no study investigated the effect of 15d-PGJ2 topical treatment against the pathological alterations caused by UVB irradiation. This was the aim of our study and we found that topical treatment with 15d-PGJ2 reduced the inflammatory and oxidative pathological modifications caused by UVB irradiation in the skin of hairless mice
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