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Deciphering the anticoccidial mechanism of Qinghao Changshan formula through network pharmacology and molecular
Dong Tian1,2, Hui Fu1, Hongxia Tao1
1Yunnan Provincial Key Laboratory of Animal Nutrition and Feed, Faculty of Animal Science and Technology, Yunnan Agricultural University, Kunming 650201, China.
Background And Aim:
Coccidiosis is a widespread protozoan disease that severely impacts poultry health and productivity. The Qinghao Changshan (QHCS) formula, composed of multiple traditional Chinese medicinal herbs, is widely used in China for coccidiosis control. Despite its proven clinical efficacy, the molecular mechanisms underlying its therapeutic action remain poorly understood. This study aimed to elucidate the active components and molecular mechanisms of QHCS against coccidiosis using an integrated approach combining network pharmacology and molecular docking.
Materials And Methods:
Active compounds of QHCS were identified from public pharmacological databases based on criteria of oral bioavailability ≥ioa and drug-likeness ≥rug-l Targets of these compounds were predicted using SwissTargetPrediction and PharmMapper, and disease-related genes were retrieved from GeneCards, DrugBank, OMIM (Online Mendelian Inheritance in Man), and Therapeutic Target Database. Overlapping targets were visualized using Venn diagrams, and protein-protein interaction (PPI) networks were constructed using STRING and Cytoscape. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to explore relevant biological functions and pathways. Molecular docking was used to validate interactions between selected active compounds (isorhamnetin, kaempferol, quercetin) and key targets (epidermal growth factor receptor [EGFR], estrogen receptor 1 [ESR1], progesterone receptor [PGR]).
Results:
Sixty-nine active compounds and 3476 potential targets of QHCS were identified, with 11 targets overlapping with 87 coccidiosis-related genes. Eight core targets-Amyloid Beta Precursor Protein, interleukin 6, TNF Receptor Associated Factor 1, Platelet Derived Growth Factor Receptor Beta, EGFR, ESR1, Erb-B2 Receptor Tyrosine Kinase 2, and PGR-were identified through PPI network analysis. GO and KEGG enrichment revealed key pathways including focal adhesion, calcium signaling, mitogen-activated protein kinase, ErbB signaling pathway, forkhead box O, and gap junction pathways. Molecular docking confirmed strong binding affinities of isorhamnetin, kaempferol, and quercetin to EGFR, ESR1, and PGR, supporting their regulatory roles in these signaling pathways.
Conclusion:
QHCS exhibits anti-coccidial activity by modulating multiple signaling pathways and molecular targets through its key bioactive constituents. These findings provide mechanistic insights into the therapeutic effects of QHCS and lay a theoretical foundation for its broader application in veterinary parasitology.
