Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation | Synapse
April 16, 2026Open Access
Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation
Key Points
The research investigates the mechanisms by which Majoon Ushba alleviates psoriatic inflammation and keratinocyte ferroptosis.
Examined the impact of Majoon Ushba on IL-17A sensitized keratinocytes
Analyzed the role of JAK-2-STAT-3 signaling
Measured inflammatory responses in an imiquimod-induced model of psoriasis
Majoon Ushba reduced IL-17A induced inflammation in keratinocytes
The treatment mitigated signs of ferroptosis
Inhibition of the JAK-2-STAT-3 pathway was observed as a mechanism of action
Abstract
In conclusion, our preliminary findings reveal a plausible mechanistic basis for the anti-psoriatic efficacy of Majoon Ushba, warranting larger clinical trials in psoriasis patient cohorts.