Cell injury associated with reactive oxygen species (ROS) has been reported in various muscular disorders. We found that a Cichorium intybus (Cii) extract reduced H(2)O(2)-induced viability loss in C2C12 myoblasts, inhibited oxidative stress-induced apoptosis and increased intracellular heat shock protein 70 (Hsp 70) expression. Cii also inhibited the level of intracellular ceramide. These results indicate that Cii may prevent skeletal muscle atrophy by inducing the expression of Hsp 70 and inhibiting the level of ceramide.

Atopic dermatitis (AD) is a chronic, allergic, and inflammatory skin disease associated with eczema and dermatitis symptoms. Our previous studies have reported that eriodictyol extract inhibits immunoglobulin E (IgE)/Ag-induced type I hypersensitivity by suppressing the activation of proinflammatory cytokines, such as interleukin-4 (IL-4), and the expression of ceramide kinase. In this study, we investigated the inhibitory effect of eriodictyol on 2,4-dinitrochlorobenzene (DNCB)-induced AD-like skin lesions in ICR mice. Treatment with 2 mg/mL eriodictyol for DNCB-induced AD-like skin lesions in ICR mice improved scratching behavior and skin severity score. Histological analysis demonstrated that thickening of the skin lesions were significantly reduced in the eriodictyol-treated group. Also, eriodictyol suppressed the DNCB-mediated elevation of IgE serum levels. These results suggest that eriodictyol may be a potential therapeutic resource for AD and an adjunctive agent to control itchiness in AD.Key words atopic dermatitis; eriodictyol; skin severity; scratching behaviorThe rate of atopic dermatitis (AD) has been increasing recently in many industrialized countries and its occurrence is usually during early infancy and childhood, but can also be in adulthood.1,2) AD is a chronic, relapsing, and inflammatory skin disease in humans and is associated with eczematous symptoms and immunoglobulin E (IgE) hyperproduction. AD is caused by a complex interrelationship among genetic, immunologic, and skin barrier dysfunction factors. 3-5)The earliest event involved in the pathogenesis of AD is considered to be a disruption of skin barrier function after scratching. Itching is a serious problem in AD patients because scratching worsens the dermatitis.6) Reduction of itching-associated scratching is the most effective therapeutic strategy for improving the quality of life for AD patients.AD is associated with the paradigm of an allergic T helper (Th) 2-mediated disease, characterized by abnormal IgE production, peripheral eosinophilia, and mast cell activation as well as upregulation of Th2 and Th1 cytokines in chronic skin lesions. 7,8) Topical steroids and immunosuppressive agents have been standard treatments for severe cases of AD. However, many patients are still worried about the long-term use of these agents and their potential adverse effects.9-11) Therefore, there is a great need for the development of new and effective therapies for AD.Eriodictyol is a unique constituent of the painted maple (Acer mono) and yerba santa (Eriodictyon californicum). Pharmacological activities attributed to eriodictyol include the control of blood vessel permeability in arthralgia and fracture, as well as antioxidant and antimicrobial effects. 12,13) Recently, our previous studies demonstrated that eriodictyol inhibits IgE-mediated allergic responses by blocking degranulation associated with ceramide kinase. Also, we showed that eriodictyol inhibits anaphylactic shock in an animal model and blocks the release of inflammatory cytokines...

Nodakenin, derived from the roots of Angelica gigas Nakai, is an important natural resource and medicinal material with anti-allergic and anti- inflammatory activities. We have previously shown that nodakenin inhibits IgE/Ag-induced degranulation in mast cells. In this study, we investigated the inhibitory effect of nodakenin on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD)- like skin lesions in ICR mice. Scratching behavior, skin severity score, blood IgE level, and skin thickness were improved in DNCB-induced AD-like ICR mice. Our results showed that nodakenin suppressed the increase of AD-like skin lesions in ICR mice. These results suggest that nodakenin may be a potential therapeutic resource for AD as well as an adjunctive agent to control itching associated with AD.

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