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.