Taraxasterol attenuates inflammatory responses in a 2,4-dinitrochlorobenzene-induced atopic dermatitis mouse model via inactivation of the MAPK and NF-κB pathways.

Atopic dermatitis (AD) is an inflammatory skin disease. Taraxasterol has anti-inflammatory effects in various pathological processes. In this study, our goal is to detect the biological functions of taraxasterol and its related mechanisms in AD development. The mouse model of experimental AD was established through application of 2',4-dintrochlorobenzene (DNCB) onto the mouse dorsal skin. Taraxasterol (2.5, 5, and 10 mg/kg) was orally administrated to AD mice. Effects of taraxasterol on AD-like skin symptoms were examined through assessment of ratios of skin lesion area/dorsal skin region, skin thickness, skin hydration, and starching number. Histopathological changes were detected by performing H&E staining. ELISA kits were obtained to measure serum TNF-α and IgE levels. RT-qPCR was conducted to measure mRNA levels of proinflammatory factors. Expression of MAPKs and NF-κB signaling was evaluated by western blotting. Taraxasterol alleviated AD-like skin symptoms (erosions, erythema, scaling, dryness, pruritus) and reduced lesion area and skin thickness in mice with DNCB-induced AD. Taraxasterol decreased epidermal thickness and serum levels of IgE and TNF-α and prevented the release of proinflammatory factors in lesion sites in of DNCB-induced AD mice. Mechanistically, taraxasterol inactivated the MAPK and NF-κB pathways. Taraxasterol alleviates AD-like skin symptoms and inflammation in a DNCB-induced AD mouse model via inactivation of the MAPK and NF-κB pathways.