Cutaneous disorders such as atopic dermatitis, psoriasis, acne vulgaris, and rosacea, together with UV-induced skin injury and photoaging, are highly prevalent conditions that involve varying contributions from dysregulated immune responses, cutaneous inflammation, oxidative stress, barrier dysfunction, microbiome alteration, and exogenous injury. However, these conditions are biologically heterogeneous and should not be regarded as a single mechanistic class. Sulforaphane, a naturally occurring isothiocyanate found primarily in broccoli and other cruciferous vegetables, has attracted interest in dermatology because of its antioxidant, cytoprotective, and context-dependent anti-inflammatory properties. Sulforaphane exerts its biological effects by modulating key signaling pathways, particularly the Keap1/Nrf2 pathway and, in some settings, NF-κB-related signaling, thereby reducing oxidative stress and inflammation, regulating immune responses, enhancing skin barrier function, and potentially influencing the cutaneous microbiome. Preclinical studies and limited human data suggest that sulforaphane may reduce erythema, edema, and other markers of cutaneous damage in selected settings. This comprehensive review explores the role of sulforaphane across heterogeneous cutaneous conditions, with emphasis on molecular mechanisms, disease-specific differences, current evidence, and discusses key translational constraints including formulation, delivery, lack of standardized dosing, and the limitations of cell culture and animal models for predicting human efficacy. Overall, sulforaphane should presently be regarded as a promising but still early-stage translational candidate in dermatology. Robust human efficacy data remain lacking for chronic inflammatory dermatoses such as psoriasis, atopic dermatitis, acne, and rosacea, whereas the strongest current human evidence relates to UV-associated skin outcomes and photoprotection.
Liu et al. (Thu,) studied this question.