Attenuation of experimentally induced atopic dermatitis in mice by sulforaphane: effect on inflammation and apoptosis

Abstract

Atopic dermatitis (AD) is characterized by progressive skin inflammation. In addition, sulforaphane is an isothiocyanate organosulfur compound from cruciferous vegetables. Sulforaphane was reported to ameliorate inflammatory responses. Therefore, this study was conducted to evaluate the protective effects of sulforaphane in AD through affecting the balance between pro-inflammatory and anti-inflammatory cytokines and to evaluate its effect on AD-induced activation of the apoptotic pathway. The method of repeated rubbing of 2,4-dinitrochlorobenzene (DNCB) on shaved dorsal skin and ears of mice was used for induction of AD. After the development of AD, part of the mice was injected with 1 mg/kg sulforaphane, subcutaneously three times weekly. Samples of skin were isolated for assessment of gene and protein expression of 8-hydroxy2′-deoxyguanosine, IgE, NFκB, TNF-α, IL-1β, IL-4, IL-10, Nrf2, and caspase-3. In addition, skin sections from different groups were stained with anti-caspase-3 antibodies. Mice in the AD group were characterized by increased gene and protein expression of 8-hydroxy2′-deoxyguanosine, IgE, NFκB, TNF-α, IL-1β, and caspase-3 associated with reduced expression of Nrf2, IL-4, and IL-10. Treatment of AD mice with sulforaphane significantly reduced the number of scratches, dermatitis score, and ear thickness. In addition, sulforaphane significantly attenuated the gene and protein expressions produced by AD. Therefore, sulforaphane alleviated AD induced in mice through inhibition of oxidative stress, oxidative DNA damage, inflammation, and apoptosis. HIGHLIGHTS Atopic dermatitis is a chronic relapsing inflammatory disease. Sulforaphane is an isothiocyanate organosulfur compound obtained from cruciferous vegetables. Sulforaphane alleviated AD induced in mice. Sulforaphane inhibits oxidative stress, oxidative DNA damage, inflammation, and apoptosis.