Investigation of the Mechanism of Action of Qinggan Yipi Formula in the Inhibition of Hepatic Fibrosis Based on Network Pharmacology and Experiments
- VernacularTitle:基于网络药理学和实验探讨清肝益脾制剂抗肝纤维化的作用机制
- Author:
Haiqing LIU
1
;
Wenjing XUE
;
Jiaqi LOU
;
Siqi WANG
;
Lurong ZHANG
;
Junping CHENG
Author Information
- Publication Type:Journal Article
- Keywords: Qinggan Yipi formula; Network pharmacology; Hepatic fibrosis; TLR4/NF-κB signaling pathway
- From: World Science and Technology-Modernization of Traditional Chinese Medicine 2025;27(8):2418-2430
- CountryChina
- Language:Chinese
- Abstract: Objective To investigate the mechanisms through which Qinggan Yipi formula(QgYp)may alleviate liver fibrosis by integrating network pharmacology with experiments.Methods The active ingredients and gene targets of QgYp,associated with liver fibrosis,were sourced from several databases,including the Traditional Chinese Medicine Systems Pharmacology Database(TCMSP),various professional chemical databases,the HERB database,the GeneCards database,and the Online Mendelian Inheritance in Man(OMIM)database.Protein-protein interaction(PPI)networks were developed using the STRING database and visualized through Cytoscape software.Furthermore,GO enrichment analysis and KEGG pathway analysis were conducted with the Metascape database,alongside molecular docking studies using the CB-DOCK 2 platform.HSC-T6 cells were used as the research model,and the MTT assay along with Western blotting were applied to evaluate cell proliferation and protein expression levels,and the expression of related proteins was also detected in the animal experiment.Results A total of 22 bioactive components and 124 gene targets were identified within the formula.Enrichment analyses revealed 896 GO entries and 123 signaling pathways,notably including the IL-7,TNF,Toll-like receptor,and NF-kappa B pathways.Molecular docking indicated that the key components of the formula exhibited a strong binding affinity with proteins involved in the TLR4/NF-κB signaling pathway.Additionally,experiments confirmed that QgYp effectively inhibited the proliferation of HSC-T6 cells induced by LPS,and the expression of α-SMA,COL-1,TLR4,IκB-α,and NF-κB p65 proteins in both HSC-T6 cells and rats with liver fibrosis decreased.Conclusion QgYp can effectively inhibit the TLR4/NF-κB signaling pathway and has a suppressive effect on the fibrosis process in hepatic stellate cells,offering a theoretical basis for its clinical application in treating liver fibrosis.
