15(R/S)-methyl-LXA(4) was well tolerated, and significantly reduced the severity of eczema. The results of this small exploratory study suggest that 15(R/S)-methyl-LXA(4) warrants further investigation in the treatment of eczema.

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p38 and JNK may be promising targets for the preservation of AQP3 expression and may be beneficial to the clinical management of diarrhoea.

Background: The clinical use of doxorubicin (DOX) is severely limited due to its cardiotoxicity. Thus, there is a need for prophylactic and treatment strategies against DOX-induced cardiotoxicity. Purpose: The purpose of this study was to develop a liquiritigenin-loaded submicron emulsion (Lq-SE) with enhanced oral bioavailability and to explore its efficacy against DOX-induced cardiotoxicity. Methods: Lq-SE was prepared using high-pressure homogenization and characterized using several analytical techniques. The formulation was optimized by central composite design response surface methodology (CCD-RSM). In vivo pharmacokinetic studies, biochemical analyses, reactive oxygen species (ROS) assays, histopathologic assays, and Western blot analyses were performed. Results: Each Lq-SE droplet had a mean particle size of 221.7 ± 5.80 nm, a polydispersity index (PDI) of 0.106 ± 0.068 and a zeta potential of −28.23 ± 0.42 mV. The area under the curve (AUC) of Lq-SE was 595% higher than that of liquiritigenin (Lq). Lq-SE decreased the release of serum cardiac enzymes and ameliorated histopathological changes in the hearts of DOX-challenged mice. Lq-SE significantly reduced oxidative stress by adjusting the levels of ROS, increasing the activity of antioxidative enzymes and inhibiting the protein expression of NOX4 and NOX2. Furthermore, Lq-SE significantly improved the inflammatory response through the mitogenactivated protein kinase (MAPK)/nuclear factor-κB (NF-κB) signalling pathway and induced cardiomyocyte apoptosis. Conclusion: Lq-SE could be used as an effective cardioprotective agent against DOX in chemotherapy to enable better treatment outcomes.

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Abstract:The mechanisms by which lipoxin A 4 (LXA 4 ) inhibit skin inflammation remain unclear. In the present studies, the ear inflammatory model was induced by topical application of mezerein. Treatment of the mouse ear with LXA 4 exhibited the inhibitory effects on oedema, neutrophil infiltration, vascular permeability, expressions of interleukin (IL)-1, IL-6 and IL-8 mRNA, DNA-binding activity of nuclear factor-jB (NF-jB), and on dermal hyperplasia. NF-jB reporter activities and nuclear translocations of NF-jB p65 in cultured keratinocytes stimulated by mezerein were inhibited by pretreatment of the cells with LXA 4 . LXA 4 reduced degradation, but not phosphorylation of IjBa in cultured keratinocytes stimulated by mezerein, suggesting that LXA 4 -attenuated IjBa degradation may restore the mezereinblocked inhibitory effects of IjB on nuclear translocation and DNA-binding activity of NF-jB. Our results demonstrated that LXA 4 displays the anti-inflammatory and anti-proliferative role on ear inflammatory model induced by mezerein and these effects were related with downregulation of DNA-binding activity of NF-jB.

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