Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disease in which skin barrier dysfunction leads to dryness, pruritus, and erythematous lesions. AD is triggered by immune imbalance and oxidative stress. Echinochrome A (Ech A), a natural pigment isolated from sea urchins, exerts antioxidant and beneficial effects in various inflammatory disease models. In the present study, we tested whether Ech A treatment alleviated AD-like skin lesions. We examined the anti-inflammatory effect of Ech A on 2,4-dinitrochlorobenzene (DNCB)-induced AD-like lesions in an NC/Nga mouse model. AD-like skin symptoms were induced by treatment with 1% DNCB for 1 week and 0.4% DNCB for 5 weeks in NC/Nga mice. The results showed that Ech A alleviated AD clinical symptoms, such as edema, erythema, and dryness. Treatment with Ech A induced the recovery of epidermis skin lesions as observed histologically. Tewameter® and Corneometer® measurements indicated that Ech A treatment reduced transepidermal water loss and improved stratum corneum hydration, respectively. Ech A treatment also inhibited inflammatory-response-induced mast cell infiltration in AD-like skin lesions and suppressed the expression of proinflammatory cytokines, such as interferon-γ, interleukin-4, and interleukin-13. Collectively, these results suggest that Ech A may be beneficial for treating AD owing to its anti-inflammatory effects.
Highlights
Atopic dermatitis (AD) is a skin disease characterized by chronic inflammation of the skin that leads to pruritus, erythematous lesions, skin barrier dysfunction, increased transepidermal water loss (TEWL), and immune-redox disturbances [1,2,3,4]
Echinochrome A (Ech A) Alleviated DNCB-Induced AD-like Skin Lesions in NC/Nga Mice
Our results are the first to show the therapeutic potential of Ech A treatment in alleviating DNCB-induced AD-like skin lesions
Summary
Atopic dermatitis (AD) is a skin disease characterized by chronic inflammation of the skin that leads to pruritus, erythematous lesions, skin barrier dysfunction, increased transepidermal water loss (TEWL), and immune-redox disturbances [1,2,3,4]. AD lesions are commonly characterized by excessive infiltration of granulated mast cells and an increased leukocyte count. Mast cells are activated by antigen-specific immunoglobulin E (IgE) through high-affinity IgE receptors (FcεRI). These cells are recruited into AD skin lesions, where they promote skin hypersensitivity reactions by releasing histamine [11,12,13]
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