The therapeutic effects of

BACKGROUND AND

aimPsoriasis is a skin disorder that leads to chronic inflammation and keratinocyte hyperproliferation. Sericin extracted from EXPERIMENTAL PROCEDURE: Imiquimod-induced skin psoriasis was established in Sprague-Dawley rats. The rats with psoriasis were divided into 6 groups (n = 5), namely, one nontreatment control group and five groups that received different treatments: sericin (2.5%, 5%, and 10%), 0.1% betamethasone, 3 μg/ml calcitriol. The treatments were administered twice daily for 7 days, followed by skin sample collection. Epidermal improvement and protein expression were evaluated using histopathological and label-free proteomic approaches and immunohistochemistry. RESULTS AND

conclusionCompared with other concentrations, 10% sericin had the desired effect of improving skin psoriasis as shown by reduced epidermal thickness, similar to the effects of betamethasone and calcitriol treatments. Anti-inflammatory activity was shown by decreased C-C motif chemokine 20 (CCL20) expression posttreatment. Proteomic observation revealed that sericin reduced cytokine production by Th17 cells by interfering with the JAK-STAT signaling pathway. Sericin treatment also resulted in a modulated immune response via upregulation of Galectin-3 (Lgals3) and downregulation of Sphingosine-1-phosphate lyase1 (Sgpl1). Sericin improved epithelial cell proliferation by upregulating Nucleoside diphosphate kinase B (Nme2). Therefore, the therapeutic effect of sericin on psoriasis correlated with a reduced immune response and attenuated epidermal proliferation, making sericin a promising approach for skin psoriasis treatment.