Ramelteon Ameliorates DNCB-Induced Atopic Dermatitis by Targeting Inflammatory and Oxidative Mechanisms in Mice

Background: Atopic dermatitis (AD) is a chronic inflammatory dermatosis characterized by immune imbalance and oxidative damage. Ramelteon, a melatoninergic receptor agonist, has recently been shown to exhibit immunomodulatory and antioxidant properties, suggesting potential therapeutic benefit in inflammatory dermatoses. Objective: The present study aimed to investigate the therapeutic effect of topically applied ramelteon in the DNCB-evoked mouse version of atopic dermatitis. Methods: 40 albino mice were indiscriminately allocated into 5 categories of 8 animals: normal controls, DNCB-model, sham, tacrolimus, and ramelteon. Ramelteon 0.25% was applied one time daily for three weeks, and the standard comparison was with tacrolimus 0.1%. Results: Ramelteon dramatically suppressed DNCB-exacerbated eczematous lesions, including decreased cumulative dermatitis scores and skin levels of TNF-α, TGF-β, IL-4, IL-13, IL-17, IL-25, IL-31, IgE, and MDA but increased SOD activity. Ramelteon also improved DNCB-exacerbated abnormalities in histopathology, including acanthosis and infiltration of immune system cells. Discussion: These results suggest the possible usefulness of ramelteon in reducing atopic dermatitis through the regulation of inflammation and oxidant pathways. Although it suppressed cytokines and oxidative markers in this study, the realization of the relative potency and long-term safety is desired. The immunomodulatory characteristics imply that it could be used as an adjuvant to present modalities. Conclusion: Through immunomodulatory and antioxidative processes, topically administered ramelteon presented probable protective qualities in DNCB-triggered atopic dermatitis, recommending it may serve as an attractive alternative and advocating for additional research to validate efficiency and safety.