Amygdalin alleviates atopic dermatitis-like skin inflammation via inhibition of Th2 immune responses

Atopic dermatitis (AD) is a chronic skin disease marked by immune dysregulation such as upregulated T helper (Th) 2 responses. While Th2-targeted therapies for AD are under development, their application is limited by side effects such as hypereosinophilia and arthritis. Amygdalin is a glucoside known for its anti-inflammatory and antioxidant effects. It is an essential component of bitter apricot kernel, traditionally utilized to alleviate inflammatory skin diseases such as boils and acne. This study focused on investigating the therapeutic effects of amygdalin on AD. Its effectiveness was evaluated both <i>in vivo</i>, using the AD mouse model induced by 2,4-dinitrochlorobenzene (DNCB) and <i>Dermatophagoides farinae</i> extract (DFE), and <i>in vitro</i>, using activated leukemia T lymphoblasts and keratinocytes. Amygdalin was shown to reduce the infiltration of immune cells in lesions and both total and DFE-specific immunoglobulin E (IgE) levels in mouse serum. Of note, it explicitly suppressed the expression of Th2 cytokines including interleukin (IL)-4, IL-5, and IL-13, as well as tumor necrosis factor (TNF)-α in ear tissues with AD induced by DNCB/DFE. These phenomena were corroborated by observations in CCRF-CEM cells, where amygdalin notably reduced the levels of IL-4 and TNF-α by inhibiting nuclear translocation of nuclear factor of activated T cells 1 and nuclear factor-κB. These findings suggest that amygdalin effectively alleviates allergic skin inflammation by suppressing the Th2 and inflammatory responses, making it a promising candidate for AD treatment.