Abstract
Forsythiae Fructus, Lonicerae Flos, and Scutellariae Radix are medicinal herbs that possess anti-inflammatory and anti-atopic effects. Hence, we investigated the effects of a mixture (ADM), containing arctigenin, hederagenin, and baicalein, which are the main compound from these herbs on atopic dermatitis (AD) skin lesions and the underlying molecular mechanisms. ADM was topically applied to dorsal skin lesions of 2,4-dinitrochlorobenzene- (DNCB-) induced ICR mice, and the expressions of proinflammatory mediators and HPA axis hormones were investigated. The topical application of 0.5% ADM significantly reduced the DNCB-induced symptoms of AD in ICR mice. Histological analysis showed that ADM exerted antiatopic effects by reducing the epidermal thickness and mast cell infiltration into skin lesions. 0.5% ADM attenuated the levels of TNF-α, IFN-γ, IL-4, and VEGF in skin lesions and serum IgE. The production of Th1-/Th2-related cytokines in splenic tissues, including TNF-α, IFN-γ, IL-12, and IL-4, were also decreased by ADM treatment. ADM diminished corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and corticosteroid (CORT) production in DNCB-induced mice. In vitro, ADM reduced the productions of TARC/CCL17, MDC/CCL22, IL-6, and ICAM-1 in TNF-α/IFN-γ- (TI-) stimulated HaCaT cells by suppressing the ERK and JNK signaling pathways. In addition, ADM inhibited corticotropin-releasing hormone/substance P- (CRH/SP-) induced VEGF production in HMC-1 cells. These results suggest that ADM may have therapeutic potential in AD by reducing inflammation and attenuating HPA axis activation.
Highlights
Atopic dermatitis (AD) is the most common chronic relapsing inflammatory skin disorder and is characterized by severe pruritus and eczematous and lichenified skin lesions
Keratinocytes in skin lesions from AD patients can produce thymus and activation-regulated chemokine (TARC)/ CCL17 and macrophage-derived chemokine (MDC)/ CCL22, which are chemoattractive for T-helper ( ) 2 cells [4], and when these cells infiltrate skin lesions, they release various inflammatory cytokines, such as interleukin (IL)-4, IL-5, IL-10, and IL-13. ese cytokines may activate the secretions of immunoglobulin E (IgE) and histamine by immune cells, which are important in the progress of allergic
To investigate the effects of a natural compound mixture (ADM) on DNCB-induced AD-like symptoms, we evaluated macroscopic signs and morphological changes in mice treated with or without ADM. e DNCB group showed increases in clinical skin symptoms as compared with the normal control group (NC) group
Summary
Atopic dermatitis (AD) is the most common chronic relapsing inflammatory skin disorder and is characterized by severe pruritus and eczematous and lichenified skin lesions. Keratinocytes form a mechanical defense against the external environment and prevent allergic sensitization to antigens. Keratinocytes maintain their barrier function by modulating proliferation/differentiation processes and by producing cytokines and chemokines [2]. Keratinocytes in skin lesions from AD patients can produce thymus and activation-regulated chemokine (TARC)/ CCL17 and macrophage-derived chemokine (MDC)/ CCL22, which are chemoattractive for T-helper ( ) 2 cells [4], and when these cells infiltrate skin lesions, they release various inflammatory cytokines, such as interleukin (IL)-4, IL-5, IL-10, and IL-13. Ese cytokines may activate the secretions of immunoglobulin E (IgE) and histamine by immune cells, which are important in the progress of allergic Keratinocytes in skin lesions from AD patients can produce thymus and activation-regulated chemokine (TARC)/ CCL17 and macrophage-derived chemokine (MDC)/ CCL22, which are chemoattractive for T-helper ( ) 2 cells [4], and when these cells infiltrate skin lesions, they release various inflammatory cytokines, such as interleukin (IL)-4, IL-5, IL-10, and IL-13. ese cytokines may activate the secretions of immunoglobulin E (IgE) and histamine by immune cells, which are important in the progress of allergic
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