Effects of Yangxue-Jiedu decoction on imiquimod-induced psoriasis-like lesions in STAT3 transgenic mice

AIM: To observe the effects of Yangxue-Jiedu (YXJD) decoction on imiquimod-induced psoriasis-like lesions in STAT3 transgenic mice.METHODS: STAT3 transgenic mice (n=24) were randomly divided into 4 groups: control group (using purified water for oral administration), model group (topical 5% imiquimod 42 mg and using purified water for oral administration), YXJD groups (topical 5% imiquimod 42 mg and using YXJD decoction for oral administration), and methotrexate (MTX) group (1 mg/kg MTX solution for oral administration, with the same topical imiquimod as model group). On day 7, the skin lesions were collected for examination. The lesions were evaluated according to the psoriasis area and severity index (PASI). The skin barrier function was evaluated by assessing oil and water components in the skin. The inflammation of psoriasis-like lesions was assessed by histological method. The expression of proliferating cell nuclear antigen (PCNA) and CD3 was assessed by immunohistochemical staining. The mRNA expression of IL-17A, IL-17C, IL-22 and RORγt was detected by real-time PCR. The levels of JAK/STAT3 pathway-related proteins in isolated T cells were determined by Western blot.RESULTS: Administration of YXJD decoction inhibited imiquimod-induced keratinocyte proliferation and infiltration of CD3⁺ T cells in psoriatic lesions, and ameliorated the epidermal barrier by up-regulation of the oil and water components in psoriatic lesions. Meanwhile, administration of YXJD decoction improved the systemic immune responses by reducing the weight of the spleen. The inflammatory cytokines IL-17A, IL-17C, IL-22 and RoRγt, and the levels of JAK/STAT3 pathway-related proteins STAT3, p-STAT3, JAK3 and p-JAK3 were decreased by administration of YXJD decoction.CONCLUSION: YXJD decoction likely alleviates imiquimod-induced psoriasis-like lesions in the STAT3 transgenic mice by inhibiting the phosphorylation of STAT3, and reducing the expression of IL-17A, IL-17C, IL-22 and RORγt.