ArticleChinese herbal medicines2024
Mechanisms of Shufeng Jiedu Capsule in treating bacterial pneumonia based on network pharmacology and experimental verification.
Article in Chinese herbal medicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Exploring possible mechanisms of antiviral effect of Shufeng Jiedu Capsule on viral pneumonia: A comprehensive analysis.Chinese herbal medicines · 2026Article
- Exploration of adverse event profiles for glofitamab: A disproportionality analysis using the FDA adverse event reporting system.PloS one · 2025Article
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10 authors.
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Abstract
Objective: The aim of this study was to investigate the underlying mechanism of Shufeng Jiedu Capsule (SFJD) for treating bacterial pneumonia (BP) Methods: Network pharmacology was used to screen the active compounds and target genes of SFJD. Then, the multi drug resistance- Results: After screening, 172 potential components of SFJD were generated, based on which we constructed an SFJD-component-target-BP interaction network. The Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment revealed that SFJD could regulate the IL-17 signaling pathway and Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway. Molecular docking showed that the potential target proteins had good combinations with the main active components. SFJD significantly reduced the mortality and prolonged survival days in lethal models. The lung index and pathological changes in the lung were also significantly decreased. SFJD could significantly decrease the expression of interleukin-17A (IL-17A), TNF receptor associated factor 6 (TRAF6), phospho-inhibitor of nuclear factor-kappa B (p-IκB)/inhibitor of NF-κB (IκB), phospho-NF-κB p65 (p-NF-κB p65), phospho-protein kinase B (p-AKT)/AKT, phospho-signal transducer and activator of transcription 3 (p-STAT3)/STAT3, phospho-signal transducer and activator of transcription 1 (p-STAT1)/STAT1, and the protein level of interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), and IL-1β. Conclusion: Combined with network pharmacology and
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