ArticleScientific reports2023
Molecular docking, network pharmacology and experimental verification to explore the mechanism of Wulongzhiyangwan in the treatment of pruritus.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 8 citations in OpenAlex.
- Elucidating the Multi-Target Anti-Pruritic Mechanism ofCurrent issues in molecular biology · 2026Article
- Rethinking network analysis in ethnopharmacology: a multi-omics and AI roadmap to overcome conceptual and methodological biases.Frontiers in pharmacology · 2026Article
- Investigating and evaluating potential antigen binding sites for monoclonal anti-HER2 antibodies: The LightDock approach.Computational and structural biotechnology journal · 2025Article
- Isoliquiritigenin Alleviates Periodontitis by Suppressing Inflammation via NF-κB Signaling Pathway of Immune Cell.Journal of inflammation research · 2025Article
- Network Pharmacology, Molecular Docking and Experimental Validation on Potential Application of Diabetic Wound Healing ofDrug design, development and therapy · 2025Article
- Forecasting the Pharmacological Mechanisms ofBiology · 2024Article
- Potential Targets and Signaling Mechanisms of Cinnamaldehyde Enhancing Intestinal Function and Nutritional Regulation in Fat Greenling (Aquaculture nutrition · 2024Article
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2 authors at 1 institution in 1 country.
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Abstract
Wulongzhiyangwan (WLZYW) is a Chinese prescription medicine for the treatment of pruritus, but its mechanism has not been clarified. The purpose of this study was to explore the mechanism of WLZYW in pruritus through network pharmacology analysis and experimental validation. The active components and corresponding targets of WLZYW were obtained from the Traditional Chinese Medicine Systematic Pharmacology (TCMSP) database. Pruritus-related targets were obtained from the GeneCards, TTD (Therapeutic Target Database), and DrugBank databases. The key compounds, core targets, main biological processes and signaling pathways related to WLZYW were identified by constructing and analyzing related networks. The binding affinity between WLZYW components and core targets was validated by AutoDock Vina software. In this study, RBL-2H3 cells were used to construct a degranulation model to simulate histamine-dependent pruritus. 10 chemical constituents, 235 targets and 3606 pruritus-related targets of WLZYW were obtained. Subsequently, 26 core targets were identified through analysis, VEGFA and AKT1 were the main candidates. A pathway enrichment analysis showed that overlapping targets were significantly enriched in the PI3K/AKT signaling pathway. A molecular docking analysis revealed tight binding of VEGF to three core compounds, kaempferol, luteolin and quercetin. Experiments showed that WZLYW inhibited mast cell degranulation, regulated VEGFa mRNA and protein expression levels by inhibiting PI3K/AKT and ERK1/2 signaling pathway activation. The mechanism of WZLYW in pruritus may be regulating VEGFa expression. Network pharmacology assays suggested that WLZYW downregulates VEGFa expression by regulating the PI3K/AKT and ERK1/2 signaling pathways in pruritis treatment.
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