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- Chunlei Yu, Fan Yang, Yu Zou, Yingbo Zhang, and Siwen Pan.
- The Institute of Medicine, Qiqihar Medical University, Qiqihar City, Heilongjiang Province, China.
- Medicine (Baltimore). 2024 Dec 6; 103 (49): e40796e40796.
BackgroundsChronic hepatitis (CH) refers to liver inflammation lasting at least 6 months caused by various factors, significantly impacting patients' daily lives. Paeoniae Radix Rubra (CS) is a classic blood-activating and stasis-dissolving herb known for its protective effects on the liver. This research seeks to investigate the underlying mechanisms by which CS treat CH, employing network pharmacology and molecular docking.MethodsThe active constituents of CS for CH treatment were identified through the TCMSP database. Targets associated with CH were gathered from GeneCards, the Therapeutic Target Database, and OMIM databases. The intersecting genes between these targets and the components of CS were considered potential therapeutic targets. Protein-protein interaction analysis was performed with the use of the STRING database and Cytoscape software, leading to the identification of core targets. These core targets underwent KEGG and GO enrichment analysis, and the top 10 pathways were chosen for building a drug-compound-target-pathway-disease' network. Finally, molecular docking was utilized to evaluate the binding affinities between the compounds and the core targets.ResultsFrom the TCMSP database, 29 compounds were screened, and 101 potential intersection targets of CS for treating CH were identified. The protein-protein interaction network analysis revealed that the core targets included EGFR, HSP90AA1, SRC, TNF, ALB, ESR1, CASP3, PTGS2, ERBB2, and FGF2. Pathway analysis indicated that CS's treatment of CH is mainly associated with the pathway in cancer. Molecular docking results indicated that Paeoniflorin and Baicalin exhibited strong binding affinity with EGFR and HSP90AA1.ConclusionThis research uncovers the possible mechanisms of CS in CH treatment, offering new avenues for future studies.Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.
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