Objectives: Atopic dermatitis (AD) is an allergic and inflammatory skin disorder caused by a combination of itching and skin sensitization by allergens. This article investigated whether cordycepin modulates AD symptoms by using an AD murine model. Material and methods: We evaluated a regulatory effect and specific molecular mechanism of cordycepin on AD induced by the repeated local exposure of 2,4-dinitrochlorobenzene to dorsal skin of mice. Blood or AD-like skin lesions samples were removed for histopathologic analysis, enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction, and Western blot analyses. Results: Oral administration of cordycepin decreased duration of scratching behavior and serum levels of histamine and immunoglobulin E increased by DNFB challenge. Cordycepin attenuated clinical symptoms and epidermis thickness of AD mice. In addition, cordycepin reduced thymic stromal lymphopoietin (TSLP), interleukin (IL)-4, IL-6, and tumor necrosis factor-α levels in the serum of AD mice. Cordycepin-attenuated infiltrations of mast cells and eosinophils with decreases in TSLP, macrophage inflammatory protein-2, and intercellular adhesion molecule-1 protein levels in AD-like skin lesions. Messenger RNA expressions of TSLP, thymus and activation-regulated chemokine/CCL17, and C–C chemokine receptor type 3 in AD-like skin lesions were also suppressed by cordycepin. Cordycepin inhibited caspase-1 expressions and activities in AD-like skin lesions. Conclusions: In conclusion, this study demonstrates that cordycepin ameliorates AD symptoms, suggesting that cordycepin might be a candidate to treat allergic skin diseases.
- atopic dermatitis
- thymic stromal lymphopoietin