ArticleDrug design, development and therapy2021
Network Pharmacology Analysis of the Mechanisms of Compound Herba Sarcandrae (Fufang Zhongjiefeng) Aerosol in Chronic Pharyngitis Treatment.
Article in Drug design, development and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 24 citations in OpenAlex.
- β-Sitosterol as an Anti-Tumour Active Component of Herba Sarcandrae Inhibits Colorectal Cancer Progression Through Up-Regulation of TBX20.Journal of cellular and molecular medicine · 2025Article
- Anti-inflammatory and analgesic effects of Kaihoujian throat spray, and therapeutic mechanism in acute pharyngitis: involvement of the NF-κB/COX-2 pathway and formula deconstruction strategy.Frontiers in pharmacology · 2025Article
- Multi-target Mechanisms of Si-Ni-San on Anxious Insomnia: An Example of Network-pharmacology and Molecular Docking Analysis.Current medicinal chemistry · 2025Article
- Role of Network Pharmacology in Prediction of Mechanism of Neuroprotective Compounds.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Exploring the Action Mechanism and Validation of the Key Pathways ofCombinatorial chemistry & high throughput screening · 2024Article
- Predictive Analysis of Yi-Gai-San's Multifaceted Mechanisms for Tremor-dominant Parkinson's DiseaseCurrent medicinal chemistry · 2024Article
- Network Pharmacology Approach for Medicinal Plants: Review and Assessment.Pharmaceuticals (Basel, Switzerland) · 2022Review
- 16SrDNA-Based Detection Technology in Patients with Chronic Pharyngitis to Analyze the Distribution Characteristics of Pharyngeal Bacteria.Journal of healthcare engineering · 2022Article
- EGFR and ERK activation resists flavonoid quercetin-induced anticancer activities in human cervical cancer cellsOncology letters · 2021Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThis study aimed to investigate the molecular mechanisms of compound herba Sarcandrae aerosol, also known as the Fufang Zhongjiefeng (FFZJF) aerosol, in treating chronic pharyngitis (CP) using network pharmacology and in vivo experimental approaches.
methodsActive compounds and putative targets of five herbs in FFZJF were identified from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform, Chemistry Database, and Swiss Target Prediction databases. The therapeutic targets of CP were obtained from OMIM, Durgbank, DisGeNT, and GAD databases. The active compounds-target networks were constructed using Cytoscape 3.6.1. The overlapping targets of FFZJF active compounds and CP targets were further analyzed using the String database to construct protein-protein interaction (PPI) network. KEGG pathway and Gene Ontology enrichment analysis was performed using the Database for Annotation, Visualization, and Integrated Discovery. The predicted targets and pathways were validated in a group A β-hemolytic streptococcus-induced rat CP model.
resultsThere were 45 active compounds identified from FFZJF and 11 potential protein targets identified for CP treatment. PPI network demonstrated that IL6, PTGS2, TLR-4, and TNF may serve as the key targets of FFZJF for the treatment of CP. The main functional pathways involving these key targets include cytokine secretion, inflammatory response, MyD88-dependent toll-like receptor signaling pathway, toll-like receptor signaling pathway, TNF signaling pathway, and NF-κB signaling pathway. In a rat CP model, the elevation of serum TNF-α, IL1β, and IL6 levels, as well as the upregulation of TLR-4, MyD88, NF-κB P65 in the pharyngeal mucosal tissues could be effectively reduced by FFZJF treatment in a dose-dependent manner.
conclusionThrough a network pharmacology approach and animal study, we predicted and validated the active compounds of FFZJF and their potential targets for CP treatment. The results suggest that FFZJF can markedly alleviate GAS-induced chronic pharyngitis by modulating the TLR-4/MyD88/NF-κB signaling pathways.
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