ArticleDrug design, development and therapy2025
Exploring the Therapeutic Mechanism of Jianpi Zhidong Decoction on Tourette Syndrome Based on Proteomics and Network Pharmacology.
Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Integrative Network Pharmacology and Transcriptomics Reveal the Mechanism of XuanShi Choudong Recipe in the Treatment of Tic Disorder.Brain and behavior · 2026Article
- The potential role of aberrant microglial synaptic pruning in the neurodevelopmental pathogenesis of tourette syndrome.Frontiers in neuroscience · 2026Review
- Network Pharmacology-Driven Sustainability: AI and Multi-Omics Synergy for Drug Discovery in Traditional Chinese Medicine.Pharmaceuticals (Basel, Switzerland) · 2025Review
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15 authors.
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Abstract
Purpose: To explore the pharmacological effects of Jianpi Zhidong Decoction (JPZDD) on Tourette Syndrome (TS) using proteomics and network pharmacology. Materials and Methods: Chemical components of JPZDD were identified via UPLC-MS/MS. Chronic restraint stress TS model was established by intraperitoneal injection of iminodipropionitrile (IDPN) for 1 week with restraint stress for 3 weeks. Sixty male SD rats were divided into control, model, Tiapride (Tia), and JPZDD groups. After the intervention of 28 days, behavioral tests, Nissl staining, Western blot, immunofluorescence, colorimetry, and ELISA were performed to evaluate the pharmacological effects of JPZDD. Proteomics and network pharmacology predicted targets, validated by Western blot. Results: JPZDD alleviated stereotypic behaviors, hippocampal pathology, and modulated glucose metabolites (GLU, pyruvate, lactate, ATP). It downregulated GLUT1, GLUT3, HK2, and LDHA levels while upregulating PDHA level. Besides, JPZDD balanced M1/M2 microglial phenotypes, reducing IL-1β and IL-6 and increasing IL-4 and IL-10. UPLC-MS/MS identified 44 active ingredients and 123 targets; proteomics revealed 28 differentially expressed proteins. GO/KEGG analysis implicated that the PI3K/AKT/mTOR pathway may be the molecular target. JPZDD inhibited PI3K, AKT, and mTOR phosphorylation. Conclusion: JPZDD (16 g·kg⁻¹·d⁻¹) alleviates motor tics, modulates microglial activation and glucose metabolism, and downregulates the PI3K/AKT/mTOR pathway, providing a mechanistic basis for its therapeutic role in TS.
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