Topical application of Rehmannia glutinosa extract inhibits mite allergen-induced atopic dermatitis in NC/Nga mice

Aim of the study: Rehmannia glutinosa is known in Asia as a traditional herbal medicine with anti-inflammatory properties. Atopic dermatitis (AD) is an inflammatory skin disease associated with enhanced T-helper 2 (Th2) lymphocyte responses to allergens that results in elevated serum IgE levels and leukocyte infiltration. Although some studies have shown that Rehmannia glutinosa extract (RGE) has anti-inflammatory and anti-allergic activities, these properties have not been demonstrated in AD. This study investigated the effectiveness of RGE as a therapeutic candidate in an AD model as well as its underlying mechanism of action. Materials and methods: The effects of RGE on mite allergen (Dermatophagoides farinae)-treated NC/Nga mice were evaluated by skin symptom severity, ear thickness, production of serum IgE and histamine, and expression of cytokines, chemokines, and adhesion molecules in the ear lesions. In addition, the levels of thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC), and regulated on activation, normal T cell expressed and secreted (RANTES) produced in both TNF-α- and IFN-γ-stimulated human keratinocytes were investigated by enzyme-linked immunosorbent assay (ELISA). Results: RGE treatment of NC/Nga mice significantly reduced dermatitis scores, ear thicknesses, and serum histamine levels. Histological analyses demonstrated decreased thickening of the epidermis/dermis as well as dermal infiltration by inflammatory cells. In the ear lesions, mRNA expression levels of IL-4, TNF-α, VCAM-1, and ICAM-1 were inhibited by RGE treatment. RGE also suppressed the production of TARC, MDC, and RANTES in both the ear lesions and keratinocytes. Conclusions: RGE inhibits the development of AD in NC/Nga mice by suppressing the expression of cytokines, chemokines, and adhesion molecules.