ArticleBrain and behavior2026
Integrative Network Pharmacology and Transcriptomics Reveal the Mechanism of XuanShi Choudong Recipe in the Treatment of Tic Disorder.
Article in Brain and behavior, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
ethnopharmacological relevanceThe Xuanshi Choudong Recipe (CDR), a classic traditional Chinese medicine (TCM) formula, has long been clinically prescribed to relieve tic disorder (TD). However, its underlying in-depth mechanism remains largely unknown. AIM OF THE STUDY: To elucidate the mechanism by which CDR exerts therapeutic effects in the treatment of TD. MATERIALS AND
methodsFour-week-old SD rats were injected intraperitoneally with apomorphine at 2 mg/kg per day to establish the model. After successful modeling, the rats were randomly divided into the model, CDR low-dose (CDRL, 6.84 g/kg), CDR medium-dose (CDRM, 13.67 g/kg), CDR high-dose (CDRH, 27.34 g/kg), and haloperidol (1 mg/kg) groups. Age-matched SD rats served as the control group. Therapeutic efficacy was evaluated using the open field test, hematoxylin and eosin (H&E) staining, and biochemical analysis. The potential mechanisms of CDR were explored using network pharmacology and transcriptomic analyses and validated by western blotting, immunofluorescence, biochemical analysis, and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining.
resultsIn this study, a total of 126 compounds were identified in CDR using liquid chromatography-mass spectrometry, with phenylpropanoids, polyketides, benzenoids, and lipids being the main components. Network pharmacology prediction revealed 265 overlapping targets between CDR and TD, with core targets including AKT1, BCL2, and IL6, and the phosphoinositide 3-kinase/protein kinase B (PI3K-AKT) signaling pathway being significantly enriched. Transcriptomic analysis showed that CDR reversed the expression of 111 genes in the striatum of TD rats, and these genes were significantly enriched in pathways related to apoptosis and the PI3K-Akt signaling pathway. Behavioral assessment demonstrated that CDR dose-dependently reduced apo-induced stereotypic behavior scores and spontaneous locomotor activity in TD rats. H&E staining indicated that CDR attenuated striatal neuronal damage. High dose CDR treatment significantly decreased the elevated levels of dopamine, 5-HT, norepinephrine, glutamate, and gamma-aminobutyric acid in the striatum (p < 0.01 or p < 0.001). Furthermore, High-dose CDR alleviated oxidative stress-induced injury by reducing reactive oxygen species and oxidized glutathione (GSSG) levels and increasing superoxide dismutase (SOD) activity, reduced glutathione (GSH) levels, and the GSH/GSSG ratio (p < 0.01 or p < 0.001). TUNEL staining and immunofluorescence results showed that CDR inhibited neuronal apoptosis in the striatum. Western blotting confirmed that CDR upregulated the phosphorylation levels of PI3K and AKT, increased the Bcl-2/Bax ratio, and downregulated caspase-3 expression, with high-dose CDR exerting the most significant effect.
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