Hydroxytyrosol ameliorates imiquimod-induced psoriasis-like dermatitis by modulating ERK and NF-κB signaling pathways in mice.

Psoriasis is a common chronic inflammatory skin disease that significantly affects patients'quality of life. There is no cure for psoriasis, and available treatments are not completely effective. We have previously found that hydroxytyrosol (HT) has anti-psoriatic effects in vitro. In the present study, we aimed to investigate the therapeutic effects of HT on psoriasis in vivo and to explore the underlying mechanisms. We explored the effects and molecular mechanisms of HT on imiquimod (IMQ)-induced psoriasis-like dermatitis in mice and an M5-induced in vitro cell model using real-time PCR, western blotting, hematoxylin-eosin staining, immunohistochemistry, and enzyme-linked immunosorbent assay. HT (10 mg/kg/d or 50 mg/kg/d, by gavage) ameliorated IMQ-induced clinical manifestations in mice. Moreover, HT ameliorated the histopathological changes and decreased the spleen index and levels of pro-inflammatory cytokines, such as interleukin (IL)-17 A, IL-23, and IL-22, in mouse serum or skin. Mechanistically, HT application inhibited the activation of ERK and NF-кB signaling in the skin samples. Consistently, in vitro analysis showed that HT significantly inhibited inflammation via ERK and NF-κB signaling in a cellular model of psoriasis. Our results indicate that HT alleviates IMQ-induced psoriasis-like dermatitis by inhibiting the ERK and NF-κB signaling pathways, suggesting that HT has a promising therapeutic application in psoriasis treatment.