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J Med Food. 2009 Oct;12(5):1004-15. doi: 10.1089/jmf.2009.0080.

Effects of orally administered Actinidia arguta (Hardy Kiwi) fruit extract on 2-chloro-1,3,5-trinitrobenzene-induced atopic dermatitis-like skin lesions in NC/Nga mice.

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Department of Dermatology, Institute of Dermatological Science, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Republic of Korea.


Atopic dermatitis (AD) is characterized by highly pruritic, chronic, relapsing inflammatory skin lesions. Furthermore, therapeutic choices are limited, especially in long-standing cases, despite its increasing prevalence. This study was performed to examine the clinical efficacy and the therapeutic mechanism underlying the effects of Actinidia arguta (hardy kiwi) fruit extract in an animal model of AD. To examine the effects of A. arguta extract on AD, 2-chloro-1,3,5-trinitrobenzene-treated NC/Nga mice were orally administered A. arguta extract (100 mg/kg/day), tacrolimus (1 mg/kg/day), or dexamethasone (3 mg/kg/day) for 8 weeks. Skin severity scores, epidermal thickening, mast cell infiltration and degranulation, total serum immunoglobulin (Ig) isotypes (IgE, IgG(1)), and cytokine (interleukin [IL]-4 and interferon [IFN]-gamma) and Toll-like receptor (TLR) (TLR-2, TLR-4, and TLR-9) expressions were examined in each of the study groups. Orally administered A. arguta extract significantly reduced clinical dermatitis severity, epidermal thickness, mast cell dermal infiltration and degranulation, and total levels of serum IgE and IgG(1). Furthermore, this suppression of total serum IgE and IgG(1) levels was accompanied by a decrease in IL-4 and an increase in IFN-gamma expression in skin and splenocytes. Interestingly, TLR-9 expression was increased by oral A. arguta extract. This study confirms that A. arguta extract has potential as a dietary therapeutic agent for the treatment of AD. Furthermore, our findings suggest that its clinical efficacy and mode of action against AD are associated with the modulation of biphasic T-helper (Th) 1/Th2 cytokines, with the inhibition of Th2-mediated IgE overproduction, and possibly with the up-regulation of TLR-9.

[Indexed for MEDLINE]

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