Abstract: Objective To investigate the therapeutic effect and underlying mechanism of Qingshi anti-itch ointment (QAO) on imiquimod-induced psoriatic skin lesions in mice. Methods Mice were randomly divided into five groups: the control, model, low-dose QAO, high-dose QAO, and positive drug groups. Skin lesions were evaluated using the PASI scoring system, and histopathological changes were observed via HE staining. The protein levels of p65, IκBα, NLRP3, ASC, and caspase-1 in skin tissue were analyzed by Western blot. RT-qPCR was used to measure the mRNA expression of p65 and IκBα. Serum levels of IL-1β, IL-18, TNF-α, and IFN-γ were quantified by ELISA. Results Compared with the control group, the model group exhibited significant erythema, scaling, and skin thickening, accompanied by increased PASI scores, elevated pro-inflammatory cytokines (IL-1β/IL-18), upregulated NLRP3/ASC/caspase-1 proteins, and activated NF-κB signaling (increased p65 and decreased IκBα). Treatment with QAO and positive drug effectively reduced PASI scores, improved skin symptoms, suppressed NLRP3 inflammasome activation, and restored the NF-κB/IκBα balance (all P＜0.05). Conclusions QAO alleviates psoriatic skin lesions in mice by inhibiting the NF-κB/NLRP3 signaling axis, thereby reducing pro-inflammatory cytokine production and inflammatory responses.

Key words: psoriasis, Qingshi anti-itch ointment, inflammatory response, skin lesions