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Abnormal expression of pro-inflammatory mediators such as cell adhesion molecules and cytokines has been implicated in various inflammatory skin diseases, including atopic dermatitis. In this study, we investigated the anti-inflammatory activity of Aronia melanocarpa concentrate (AC) and its action mechanisms using in vivo and in vitro skin inflammation models. Topical application of AC on mouse ears significantly suppressed 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ear edema formation, as judged by measuring ear thickness and weight, and histological analysis. Topical administration of AC also reduced the expression of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 in TPA-stimulated mouse ears. Pretreatment with AC suppressed TNF-α-induced ICAM-I expression and subsequent monocyte adhesiveness in human keratinocyte cell line HaCaT. In addition, AC significantly decreased intracellular reactive oxygen species (ROS) generation as well as mitogen-activated protein kinase (MAPK) activation in TNF-α-stimulated HaCaT cells. AC and its constituent cyanidin 3-glucoside also attenuated TNF-α-induced IKK activation, IκB degradation, p65 phosphorylation/nuclear translocation, and p65 DNA binding activity in HaCaT cells. Overall, our results indicate that AC exerts anti-inflammatory activities by inhibiting expression of pro-inflammatory mediators in vitro and in vivo possibly through suppression of ROS-MAPK-NF-κB signaling pathways. Therefore, AC may be developed as a therapeutic agent to treat various inflammatory skin diseases.

Melatonin is known to have a neuroprotective effect by preventing epileptic seizures, which are normally induced by cyanide. To demonstrate the neuroprotective function of melatonin, we examined cell death and changes in plasma melatonin level in KCN-treated mice. Neuronal cell death is shown in substantial nigra of KCN-treated groups. In melatonin-treated groups, this cell death decreased in substantia nigra. Plasma melatonin level at 12:00 was significantly decreased to 52.6% after KCN injection as compared to the normal group. In contrast, melatonin level was significantly decreased (74.5%) in KCN + melatonin group. Melatonin level at 24:00 was significantly decreased to 57.0% after KCN injection and also significantly decreased to 81.0% in KCN-melatonin group as compared to the normal group. Results from the present study suggest that melatonin prevents neuronal cell death in KCN-induced brain.

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