XIAO Jia-ning, XUE Shan-shan, NI Ping-min, WANG Zhuo, WU Yong-jun. Study on the Mechanism of Biyuan Heji in the Treatment of Acute Sinusitis Based on NF-κB Signal Pathway[J]. Journal of Nanjing University of traditional Chinese Medicine, 2022, 38(3): 247-253. DOI: 10.14148/j.issn.1672-0482.2022.0247
Citation: XIAO Jia-ning, XUE Shan-shan, NI Ping-min, WANG Zhuo, WU Yong-jun. Study on the Mechanism of Biyuan Heji in the Treatment of Acute Sinusitis Based on NF-κB Signal Pathway[J]. Journal of Nanjing University of traditional Chinese Medicine, 2022, 38(3): 247-253. DOI: 10.14148/j.issn.1672-0482.2022.0247

Study on the Mechanism of Biyuan Heji in the Treatment of Acute Sinusitis Based on NF-κB Signal Pathway

  •   OBJECTIVE  Based on NF-κB signaling pathway to explore the mechanism of Biyuan Heji (BYHJ) in The Treatment of Acute Sinusitis.
      METHODS  Through TCMSP and Uniprot database, the effective active components and corresponding target genes of each drug in BYHJ were obtained. With the help of Genecards, the target genes related to acute sinusitis (ARS), and the intersection of the two target genes were retrieved. Metascape for GO and KEGG data was used. Cytoscape software was used to construct the network diagram of "Drug-Active ingredient-Target", and the plug-in, "Bisogenet", was used to create PPI network and analyze the imformation. At the same time, animal experiments were carried out to verify NF-κB signaling pathway.
      RESULTS  66 active components and 239 corresponding target genes of BYHJ, 2 236 target genes related to ARS and 141 intersection genes. The main active components were quercetin, kaempferol, β-sitosterol, etc. GO and KEGG suggested that BYHJ cured ARS via NF-κB signaling pathway, cancer pathway and TNF signaling pathway and so forth.In animal experiments, after gavage administration of BYHJ, the level of IL-1β、IL-6、IL-8、TNF-α、NF-κBp50、NF-κBp65, related to NF-κB signaling pathway, decreased in vary degrees in ARS rats.
      CONCLUSION  BYHJ can reduce the inflammatory response of ARS rats, and its mechanism is to intervene NF-κB signaling pathway by inhibiting the expression of inflammatory factors.
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