Exploring the mechanism ofkaji-ichigoside F1on bacterial pneumonia based on the network pharmacology and transcriptome

  1. Junlin Yang
  2. Xi Yang
  3. Liping Wu
  4. Cheng Min
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Abstract

Objective

To explore the anti-inflammatory mechanism ofkaji-ichigoside F1against bacterial pneumonia based on transcriptomics and network pharmacology.

Method

Network pharmacological was used to analyse the potential target genes ofkaji-ichigoside F1action on bacterial pneumonia; molecular docking was used to analyse the docking binding energy ofkaji-ichigoside F1with key target genes; RAW264.7 macrophages were treated withklebsiella pneumoniaefluid and givenkaji-ichigoside F1intervention, the expression of inflammatory factors IL-1β, IL-6, TNF-α and IL-10 were dectected by qRT-PCR; transcriptomic analysis was performed to obtain differentially expressed genes, and relevant signaling pathways.

Result

Network pharmacological analysis showed that the five the key target genes forkaji-ichigoside F1-bacterial pneumonia interaction were were TLR4, NFKB1, STAT3, IL1B, and JUN; molecular docking results ofkaji-ichigoside F1with key target genes showed the docking binding energy ranging from -5.9 to -8.4 kcal/mol;kaji-ichigoside F1can reduce theklebsiella pneumoniaeinduced inflammatory response of macrophages, manifested with reducing the mRNA expression of pro-inflammatory factors IL-1β, IL-6 and TNF-α, and increase the mRNA expression of anti-inflammatory factor IL-10; transcriptomics analysis showed that the signaling pathways involved were mainly the TLR signaling pathway and NFKB signaling pathway.

Conclusion

This study showed thatkaji-ichigoside F1alleviates bacterial pneumonia by targeting TLR and NFKB signaling pathways, rebalancing macrophage polarization with suppressing pro-inflammatory cytokines and increasing anti-inflammatory cytokines, highlightingkaji-ichigoside F1as a novel agent for combating bacterial infections.

Graphic abstract

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