Abstract
Background and purpose:
Psoriasis is an inflammatory skin disease of chronic recurrence mediated by the interaction between IL-17 and keratinocytes, which sustains a vicious circle of inflammation. Safe and effective natural medicine is a potential strategy for the clinical treatment of psoriasis. Given its prominent anti-proliferative and anti-inflammatory properties, we investigated the mechanism of allicin improving psoriasis.
Experimental approach:
The pharmacodynamic study was estimated on mice after topical administration of allicin with psoriasis-like lesions induced by imiquimod. The skin sensitization test was evaluated on guinea pigs. The toxicology study and skin irritation test were assessed by consecutively topical allicin alone on the skin of rabbits. RNA-seq probed transcriptomic changes following the action of allicin. Western Blot explored the mechanism of allicin in the interaction between IL-17A and keratinocytes. Changes in inflammatory factors expression were analyzed by qPCR and immunohistochemistry.
Key results:
Allicin significantly improved the epidermal structure by inhibiting excessive proliferation and evasion of apoptosis of keratinocytes. Furthermore, allicin reduced the secretion of inflammatory cytokines (IL-17A/F, IL-22, IL-12, IL-20), chemokines (CXCL2, CXCL5, CCL20), and antibacterial peptides (S100a8/9). Mechanistically, allicin directly inhibited the IL-17-induced TRAF6/MAPK/NF-κB and STAT3/NF-κB signaling cascades in keratinocytes, thus breaking the positive inflammation feedback and alleviating imiquimod-induced psoriasis-like dermatitis in mice. Importantly, topical administration of allicin did not cause skin allergy, and the safety and adaptability of long-term application were verified.
Conclusions and implications:
Interfering with IL-17 signaling in keratinocytes with allicin is a promising strategy for treating psoriasis, given its safety and effectiveness.
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