Skip to main content
ImmuneCited

Molecular Mechanisms Underlying the Effects of Bimin Kang Mixture on Allergic Rhinitis: Network Pharmacology and RNA Sequencing Analysis.

Li-Jie Qi, Ren-Zhong Wang, Shang Gao, Xiang-Jing Chen, Xin Zhang et al.
Other BioMed research international 2022 5 citazioni
PubMed DOI PDF
<\/script>\n
`; }, get iframeSnippet() { const domain = 'immunecited.com'; const params = 'pmid\u003D36337846'; return ``; }, get activeSnippet() { return this.method === 'script' ? this.scriptSnippet : this.iframeSnippet; }, copySnippet() { navigator.clipboard.writeText(this.activeSnippet).then(() => { this.copied = true; setTimeout(() => { this.copied = false; }, 2000); }); } }" @keydown.escape.window="open = false" @click.outside="open = false">

Embed This Widget

Style



      
      
    

Widget powered by . Free, no account required.

Study Design

Tipo di studio
Other
Popolazione
None
Intervento
Molecular Mechanisms Underlying the Effects of Bimin Kang Mixture on Allergic Rhinitis: Network Pharmacology and RNA Sequencing Analysis. None
Comparatore
None
Esito primario
None
Direzione dell'effetto
Mixed
Rischio di bias
Unclear

Abstract

BACKGROUND: Allergic rhinitis (AR) is a highly prevalent chronic inflammatory disease of the respiratory tract. Previous studies have demonstrated that Bimin Kang Mixture (BMK) is effective in alleviating AR symptoms and reducing the secretion of inflammatory factors and mucin; however, the precise mechanisms underlying these effects remain unclear. METHODS: We built target networks for each medication component using a network pharmacology technique and used RNA-seq transcriptome analysis to screen differentially expressed genes (DEGs) for AR patients and control groups. The overlapping targets in the two groups were assessed using PPI networks, GO, and KEGG enrichment analyses. The binding ability of essential components to dock with hub target genes was investigated using molecular docking. Finally, we demonstrate how BMK can treat AR by regulating the NF-κB signaling pathway through animal experiments. RESULTS: Effective targets from network pharmacology were combined with DEGs from RNA-seq, with 20 intersections as key target genes. The construction of the PPI network finally identified 5 hub target genes, and all hub target genes were in the NF-κB signaling pathway. Molecular docking suggests that citric acid, deoxyandrographolide, quercetin, luteolin, and kaempferol are structurally stable and can spontaneously attach to IL-1β, CXCL2, CXCL8, CCL20, and PTGS2 receptors. Animal experiments have shown that BMK inhibits NF-κB transcription factor activation, reduces the expression of proinflammatory cytokines and chemokines IL-1β, CXCL2, IL-8, and COX-2, and exerts anti-inflammatory and anti-allergic effects. CONCLUSION: BMK by regulating the NF-κB signaling pathway improves inflammatory cell infiltration, regulates mucosal immune balance, and reduces airway hypersensitivity. These findings provide theoretical support for the clinical efficacy of BMK for AR treatment.

TL;DR

Findings provide theoretical support for the clinical efficacy of BMK for AR treatment by regulating the NF-κB signaling pathway, which improves inflammatory cell infiltration, regulates mucosal immune balance, and reduces airway hypersensitivity.

Full Text

PDF
Loading PDF...

Used In Evidence Reviews

Similar Papers