Pathology, research and practice · 2026
Uncovering the anti-inflammatory mechanisms of compound Muniziqi granule against psoriasis by network analysis and experimental evaluation in vivo.
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Fu Cuiying, Yang Juexi, Lin Xiner, Chen Pu, Dai Yan, Sun Yan, Dou Xiaoke, Wu Yan, Zhang Song
Аннотация
OBJECTIVE: To evaluate the efficacy of Compound Muniziqi Granule (MNZQ) and explore its mechanisms in an imiquimod (IMQ)-induced psoriasiform mouse model.
METHODS: IMQ cream was applied to dorsal skin to induce lesions. Treatment groups received MNZQ by oral gavage at 1.8, 3.6, and 5.4 g/kg/day, or methotrexate (MTX, 10 mg/kg/week). MNZQ was chemically characterized by UPLC-MS/MS to profile its metabolites. The curated metabolite set was then used for network analysis and molecular docking. Predicted targets and pathways were evaluated by in vivo outcomes (PASI scores and H&E histology) and bench validation, including RT-qPCR (Il17a/Il22), flow cytometry (Th17, γδ T17), and Western blotting for STAT3, AKT, mTOR, and their phosphorylated forms.
RESULTS: MNZQ significantly improved clinical and histological indices. As a hypothesis-generating step, in silico network analysis and molecular docking prioritized Th17 differentiation and the IL-17, JAK-STAT, and PI3K-AKT pathways. Consistent with these predictions, MNZQ was associated with lower frequencies of Th17 and γδ T17 cells in skin, spleen, and draining lymph nodes, and with reduced Il17a/Il22 transcripts in lesions and draining nodes (no clear dose-response). At the protein level, lesional skin showed decreased phosphorylation of STAT3, AKT, and mTOR.
CONCLUSION: The findings indicate that MNZQ exerts anti-psoriatic efficacy in vivo, concurrent with decreases in γδ T17/Th17 cells frequencies and attenuation of the pro-inflammatory JAK-STAT3 and PI3K-AKT-mTOR signaling pathways.
METHODS: IMQ cream was applied to dorsal skin to induce lesions. Treatment groups received MNZQ by oral gavage at 1.8, 3.6, and 5.4 g/kg/day, or methotrexate (MTX, 10 mg/kg/week). MNZQ was chemically characterized by UPLC-MS/MS to profile its metabolites. The curated metabolite set was then used for network analysis and molecular docking. Predicted targets and pathways were evaluated by in vivo outcomes (PASI scores and H&E histology) and bench validation, including RT-qPCR (Il17a/Il22), flow cytometry (Th17, γδ T17), and Western blotting for STAT3, AKT, mTOR, and their phosphorylated forms.
RESULTS: MNZQ significantly improved clinical and histological indices. As a hypothesis-generating step, in silico network analysis and molecular docking prioritized Th17 differentiation and the IL-17, JAK-STAT, and PI3K-AKT pathways. Consistent with these predictions, MNZQ was associated with lower frequencies of Th17 and γδ T17 cells in skin, spleen, and draining lymph nodes, and with reduced Il17a/Il22 transcripts in lesions and draining nodes (no clear dose-response). At the protein level, lesional skin showed decreased phosphorylation of STAT3, AKT, and mTOR.
CONCLUSION: The findings indicate that MNZQ exerts anti-psoriatic efficacy in vivo, concurrent with decreases in γδ T17/Th17 cells frequencies and attenuation of the pro-inflammatory JAK-STAT3 and PI3K-AKT-mTOR signaling pathways.