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<p>Chronic rhinosinusitis with nasal polyps (CRSwNP) is a persistent inflammatory disease involving complex cytokine networks and signaling pathways. Triptolide (TP) has known anti-inflammatory properties, but its precise mechanisms in CRSwNP remain unclear. This study employed network pharmacology, bioinformatics, clinical samples, and in vitro cellular experiments to investigate TP’s effects and potential mechanisms. The results showed that CXCL8 significantly promotes inflammation by activating the AKT/NF-κB pathway, thereby upregulating cytokines such as TNF-α, IL-1β, and IL-6, while simultaneously downregulating the expression of epithelial barrier proteins such as ZO-1, E-cadherin, and Occludin. This reduces cell resistivity and increases cell permeability. TP effectively reversed CXCL8-induced increases in CXCR2 and CXCR4 expression, inhibited the AKT/NF-κB pathway, and reduced pro-inflammatory cytokine production. Additionally, TP improves CXCL8-induced nasal mucosal barrier function by restoring the expression of proteins associated with the cellular barrier function of nasal mucosal cells. These findings suggest that TP may alleviate CRSwNP-associated inflammation and barrier dysfunction by affecting the CXCL8/CXCR2/CXCR4 axis and NF-κB signaling, highlighting its potential as a therapeutic agent for managing CRSwNP.</p>

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Triptolide alleviates inflammation and barrier dysfunction in chronic rhinosinusitis with nasal polyps by affecting the CXCL8/CXCR2/CXCR4 axis and AKT/NF-κB signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月25日

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  • Jinyun Wu,
  • Tian Zhang,
  • Ying Jin,
  • Guodong Yu

摘要

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a persistent inflammatory disease involving complex cytokine networks and signaling pathways. Triptolide (TP) has known anti-inflammatory properties, but its precise mechanisms in CRSwNP remain unclear. This study employed network pharmacology, bioinformatics, clinical samples, and in vitro cellular experiments to investigate TP’s effects and potential mechanisms. The results showed that CXCL8 significantly promotes inflammation by activating the AKT/NF-κB pathway, thereby upregulating cytokines such as TNF-α, IL-1β, and IL-6, while simultaneously downregulating the expression of epithelial barrier proteins such as ZO-1, E-cadherin, and Occludin. This reduces cell resistivity and increases cell permeability. TP effectively reversed CXCL8-induced increases in CXCR2 and CXCR4 expression, inhibited the AKT/NF-κB pathway, and reduced pro-inflammatory cytokine production. Additionally, TP improves CXCL8-induced nasal mucosal barrier function by restoring the expression of proteins associated with the cellular barrier function of nasal mucosal cells. These findings suggest that TP may alleviate CRSwNP-associated inflammation and barrier dysfunction by affecting the CXCL8/CXCR2/CXCR4 axis and NF-κB signaling, highlighting its potential as a therapeutic agent for managing CRSwNP.