ArticleDrug design, development and therapy2024
Therapeutic Effects of Qingchang Tongluo Decoction on Intestinal Fibrosis in Crohn's Disease: Network Pharmacology, Molecular Docking and Experiment Validation.
Article in Drug design, development and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Walnut Peptide KG-7 Alleviates Scopolamine-Induced Memory Deficits and Enhances Paracellular Transport via Tight Junction Modulation in a Mouse Model.Foods (Basel, Switzerland) · 2026Article
- Deciphering the anti-atherosclerotic mechanisms of Danggui-Chuanxiong herb pair: a synergistic approach combining computational prediction andFrontiers in cardiovascular medicine · 2026Article
- Unraveling the Mechanisms ofPlants (Basel, Switzerland) · 2025Article
- Inflammation-fibrosis interplay in inflammatory bowel disease: mechanisms, progression, and therapeutic strategies.Frontiers in pharmacology · 2025Review
- The Role of Gut Microbiota on Intestinal Fibrosis in Inflammatory Bowel Disease and Traditional Chinese Medicine Intervention.Journal of inflammation research · 2025Review
- Research Progress on the Diagnosis and Treatment of Intestinal Fibrosis in Crohn's Disease with Traditional Chinese and Western Medicine.Iranian journal of pharmaceutical research : IJPRArticle
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Authors and funding
10 authors.
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Abstract
Background: Qingchang Tongluo Decoction (QTF) is clinically used for the treatment of intestinal fibrosis in Crohn's Disease (CD). However, the role of QTF in CD-associated fibrosis and its potential pharmacological mechanism remains unclear. Purpose: The objective of this study was to elucidate the potential mechanism of QTF in treating CD-associated fibrosis, employing a combination of bioinformatics approaches - encompassing network pharmacology and molecular docking - complemented by experimental validation. Methods: To investigate the material basis and potential protective mechanism of QTF, a network pharmacology analysis was conducted. The core components and targets of QTF underwent molecular docking analysis to corroborate the findings obtained from network pharmacology. In vitro, a colon fibrotic model was established by stimulating IEC-6 cells with 10 ng/mL of transforming growth factor(TGF-β1). In vivo, an intestinal fibrosis model was induced in BALB/c mice by TNBS. The role of QTF in inhibiting the TGF-β1/Smad signaling pathway was investigated through RT-qPCR, Western blotting, immunohistochemistry staining, and immunofluorescence staining. Results: Network pharmacology analysis revealed that QTF could exert its protective effect. Bioinformatics analysis suggested that Flavone and Isoflavone might be the key components of the study. Additionally, AKT1, IL-6, TNF, and VEGFA were identified as potential therapeutic targets. Furthermore, experimental validation and molecular docking were employed to corroborate the results obtained from network pharmacology. RT-qPCR, Immunofluorescence, and Western blotting results demonstrated that QTF significantly improved colon function and inhibited pathological intestinal fibrosis in vivo and in vitro. Conclusion: Through the application of network pharmacology, molecular docking, and experimental validation, QTF could be confirmed to inhibit the proliferation of intestinal fibroblasts associated with CD and reduce the expression of Collagen I and VEGFA. This effect is achieved through the attenuation of ECM accumulation, primarily via the inhibition of the TGF-β1/Smad signaling pathway.
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