Rutaecarpine inhibited imiquimod-induced psoriasis-like dermatitis via inhibiting the NF-κB and TLR7 pathways in mice

Abstract

Psoriasis is a chronic, immune-mediated inflammatory skin disease. As psoriasis rarely occurs in nonhuman animals, the lack of an ideal animal model reflecting the histopathological and molecular immunological characteristics of psoriasis remains an urgent issue. In the present study, an imiquimod-induced psoriasis-like dermatitis mouse model was constructed under natural immune conditions and verified by evaluations of the Psoriasis Area and Severity Index (PASI) score and Baker score, H&E staining, immunohistochemical examination of the CD3 and Gr1 levels, measurement of plasmacytoid dendritic cell- (pDC) and Th17-associated cytokine levels, and evaluation of p65 phosphorylation and TLR7 expression. Moreover, rutaecarpine (RUT), the main active ingredient in the traditional Chinese medicine Wu-Zhu-Yu, could improve psoriasis-like dermatitis through effects on pDC- and Th17-associated cytokines through NF-κB and toll-like receptor 7 (TLR7) signaling. Taken together, the imiquimod-induced psoriasis-like dermatitis mouse model can be regarded as an ideal model for evaluating psoriasis pathogenesis and antipsoriatic drugs. We provided theoretical and experimental evidence for the clinical application of RUT in psoriasis.

Keywords: Cytokines; NF-κB signaling; Psoriasis-like dermatitis; Rutaecarpine; TLR7 signaling pathway.