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Background and Purpose: Epoxyeicosatrienoic acids (EETs) and other epoxy fatty acids (EpFA) are lipid mediators that are rapidly inactivated by soluble epoxide hydrolase (sEH). Uncontrolled and chronic inflammatory disorders fail to sufficiently activate endogenous regulatory pathways, including the production of specialized proresolving mediators (SPMs). Here, we addressed the relationship between SPMs and the EET/sEH axis and explored the effects of sEH inhibition on resolving macrophage phenotype.Experimental Approach: Mice were treated with a sEH inhibitor, EETs, or sEH inhibitor + EETs (combination) before ligature placement to induce experimental periodontitis. Using RT-qPCR, gingival samples were used to examine SPM receptors and osteolytic and inflammatory biomarkers. Maxillary alveolar bone loss was quantified by micro-CT and methylene blue staining. SPM levels were analysed by salivary metabolo-lipidomics. Gingival macrophage phenotype plasticity was determined by RT-qPCR and flow cytometry. Effects of sEH inhibition on macrophage polarization and SPM production were assessed with bone marrow-derived macrophages (BMDMs).

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The present study examined the efficacy of the topical 15d-PGJ 2 -poloxamer 407 hydrogel in an atopic dermatitis (AD) animal model. The 15d-PGJ 2 hydrogel was prepared and characterized. The examined rats possessed AD-Like cutaneous lesions, which were induced using 2,4-dinitrochlorobenzene, the rats were then treated with a hydrogel vehicle, 15d-PGJ 2 hydrogel or tacrolimus for 14 days. The rats were sacrificed and blood samples were collected to quantify the IgE levels. Subsequently, skin biopsies were stained with toluidine blue to identify mast cells and immunohistochemistry was performed for ROR-γt and TNF-α. Histological analyses demonstrated that 15d-PGJ 2 hydrogel significantly decreased mast cell infiltration (P<0.05) when compared with the AD-group. Tacrolimus at 0.1% exhibited decreased mast cell infiltration; however, this difference was not statistically significant from the AD-group. Topical 15d-PGJ 2 hydrogel and Tacrolimus 0.1% significantly reduced the serum levels of IgE (P<0.05) compared with the AD-group. Immunohistochemistry revealed a significant decrease in ROR-γt and TNF-α positive cell expression (P<0.05) in the 15d-PGJ 2 hydrogel group compared with the AD-group. In summary, topical administration of 15d-PGJ 2 hydrogel had a beneficial effect on AD symptoms, suggesting that this formulation may be a useful strategy for the treatment of AD.

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