Conclusion
This study elucidated the molecular mechanism of allicin in improving IMQ-induced psoriatic lesions in mice. In this regard, allicin inhibits the innate immune response to external stimuli in psoriatic lesions, resulting in reduced expression of pro-inflammatory cytokines and chemokines. Furthermore, allicin treatment mitigates psoriasis progression by inhibiting the TRAF6/MAPK/NF-κB and STAT3/NF-κB signaling pathways and activating the apoptotic signaling cascade in keratinocytes. Overall, our data substantiated that interfering with IL-17 signaling in keratinocytes with allicin is a promising strategy for treating psoriasis, given its safety and effectiveness.