Topical Administration of 15-Deoxy-Δ^12,14-Prostaglandin J₂ Using a Nonionic Cream: Effect on UVB-Induced Skin Oxidative, Inflammatory, and Histopathological Modifications in Mice

Figure 10

Schematic representation of the effects of topical formulation containing 15d-PGJ₂ (TFcPGJ₂) against skin alterations upon UVB irradiation. UVB causes inflammatory disease signs such as skin edema as well as pathological alterations in the skin including sunburn cell formation, an increase of mast cell counts, thickening of the epidermis, and collagen degradation. These phenomena are explained by the induction of neutrophil recruitment observed as myeloperoxidase (MPO) activity, metalloproteinase-9 (MMP-9) activity, reactive oxygen species (ROS) production, depletion of endogenous antioxidants, enhanced mRNA expression of enzymes involved in the production of ROS and inflammatory mediators such as gp91^phox and cyclooxygenase-2 (COX-2), and cytokine production (TGF-β and IL-6). All these UVB pathological modifications in the skin were inhibited by TFcPGJ₂ and unaltered by an unloaded topical formulation (uTF—not mentioned in the schematic figure).