AI Article Synopsis

  • The study aimed to explore how Shufeng Jiedu Capsule (SFJD) treats bacterial pneumonia through network pharmacology and experimental methods.
  • Researchers found 172 active components in SFJD and built a network connecting these components with target genes related to bacterial pneumonia, highlighting its effects on the IL-17 and JAK/STAT signaling pathways.
  • SFJD showed promising results by reducing mortality in mouse models of pneumonia and decreasing harmful inflammatory markers, indicating its potential as a treatment for bacterial pneumonia.*

Article Abstract

Objective: The aim of this study was to investigate the underlying mechanism of Shufeng Jiedu Capsule (SFJD) for treating bacterial pneumonia (BP) based on network pharmacology and experimental verification study.

Methods: Network pharmacology was used to screen the active compounds and target genes of SFJD. Then, the multi drug resistance- (MDR-PA) mice lethal model and MDR-PA pneumonia model were established to evaluate the therapeutic effects and underlying mechanisms of SFJD. Western blot and ELISA were used to determinate the protein expression level of the IL-17 signaling pathway and JAK/STAT signaling pathway.

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 study, it was found that SFJD exerted its therapeutic effects on BP by inhibiting the IL-17 pathway and JAK/STAT signaling pathway. This study provides new evidence for SFJD in treatment of BP.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11589334PMC
http://dx.doi.org/10.1016/j.chmed.2024.01.002DOI Listing

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