Arch Dermatol Res. 2024 Dec 14;317(1):115. doi: 10.1007/s00403-024-03550-8.
ABSTRACT
Psoriasis is a chronic, relapsing, inflammatory skin disease that is caused by the immune system. Amygdalin possesses immune-modulating and anti-inflammatory effects. To explore the possible effects of amygdalin on psoriasis and its pathogenesis of action, we examined the effects of amygdalin on imiquimod-induced psoriasis, tape-stripping-induced skin barrier disruption, and investigated the potential mechanism of action in vitro. The fact that amygdalin could reduce the thickness of the epidermis and inflammatory cell infiltration in two animal models inhibited the production of IL-1β, IL-6, and TNF-a, and the expression of filaggrin, involucrin, and keratin10 was increased. Also, in IL-17 A and TNF-α induced HaCaT, amygdalin inhibits the expression of IL-6, IL-1β, and TNF-a, promoting the expression of skin barrier recovery-related proteins flaggrin, involucrin, and keratin10. Combined in vivo and in vitro experiments suggest that amygdalin modulates inflammation and the skin barrier in psoriasis. The same study also conducted a preliminary mechanistic exploration and found that amygdalin inhibited the phosphorylation of the p38MAPK signaling pathway. In conclusion, Amygdalin can alleviate psoriasis lesions and improve skin barrier impairment, and the research provides an experimental basis for its future development as a drug candidate for psoriasis therapy.
PMID:39673560 | DOI:10.1007/s00403-024-03550-8
Von Automat