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已发表论文
鱼腥草素钠对急性鼻窦炎的双重作用：抗菌作用及通过 p38 MAPK/ERK 通路修复上皮屏障
Authors Fang Y, Zhou H, Li W, Bai L, Sun X, He K, Xue S, Wu Y
Received 13 May 2025
Accepted for publication 20 September 2025
Published 29 September 2025 Volume 2025:18 Pages 13433—13452
DOI https://doi.org/10.2147/JIR.S539966
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Tara Strutt
Yang Fang, Huixia Zhou, WeiYi Li, Lu Bai, Xinchen Sun, KaiYuan He, Shanshan Xue, Yongjun Wu
Department of Otolaryngology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People’s Republic of China
Correspondence: Shanshan Xue, Email 390429607@qq.com Yongjun Wu, Email wooyongjun@126.com
Background: Houttuynia cordata Thunb, a traditional medicinal herb, is the source of sodium houttuyfonate (SH), a stabilized derivative with antibacterial, antiviral, and anti-inflammatory activities. Acute rhinosinusitis (ARS) comprises viral, post-viral, and bacterial forms; bacterial ARS causes severe inflammation and epithelial barrier disruption. Despite wide clinical use, the mechanisms of SH in ARS remain unclear.
Methods: Network pharmacology was applied to identify SH-associated targets and pathways. An ARS rat model was induced by inserting Staphylococcus aureus–soaked Merocel sponges into the nasal cavity. Rats received low, medium, or high doses of SH, with control and positive drug groups. Symptom scoring, CT, histopathology, hematology, ELISA, qRT-PCR, and immunohistochemistry were conducted. In vitro, human nasal epithelial cells (HNEpCs) were stimulated with lipopolysaccharide (LPS) and treated with SH, with or without MAPK modulators SB203580 (inhibitor) or Anisomycin (activator). Cell viability, cytokine expression, and ERK/p38 MAPK phosphorylation were assessed.
Results: SH improved nasal symptoms, reduced epithelial injury, and normalized nasal pH in ARS rats. It downregulated IL-1β, IL-6, TNF-α, and ICAM-1 while upregulating IL-4. Transmission electron microscopy showed restoration of ciliary and mitochondrial integrity. In HNEpCs, 60 μM SH was optimal by CCK-8 assay. In LPS-stimulated cells, SH suppressed IL-1β/IL-6 mRNA and inhibited ERK and p38 MAPK phosphorylation; these effects were reversed by Anisomycin, confirming pathway involvement.
Conclusion: SH alleviates sinonasal inflammation in ARS by inhibiting bacterial activity and restoring epithelial integrity through p38 MAPK/ERK suppression. These findings support SH as a potential therapy for upper airway inflammatory diseases.
Keywords: sodium houttuyfonate, acute rhinosinusitis, houttuynia cordata, p38 MAPK/ERK signaling, inflammation, ethnopharmacology
Department of Otolaryngology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People’s Republic of China
Correspondence: Shanshan Xue, Email 390429607@qq.com Yongjun Wu, Email wooyongjun@126.com
Background: Houttuynia cordata Thunb, a traditional medicinal herb, is the source of sodium houttuyfonate (SH), a stabilized derivative with antibacterial, antiviral, and anti-inflammatory activities. Acute rhinosinusitis (ARS) comprises viral, post-viral, and bacterial forms; bacterial ARS causes severe inflammation and epithelial barrier disruption. Despite wide clinical use, the mechanisms of SH in ARS remain unclear.
Methods: Network pharmacology was applied to identify SH-associated targets and pathways. An ARS rat model was induced by inserting Staphylococcus aureus–soaked Merocel sponges into the nasal cavity. Rats received low, medium, or high doses of SH, with control and positive drug groups. Symptom scoring, CT, histopathology, hematology, ELISA, qRT-PCR, and immunohistochemistry were conducted. In vitro, human nasal epithelial cells (HNEpCs) were stimulated with lipopolysaccharide (LPS) and treated with SH, with or without MAPK modulators SB203580 (inhibitor) or Anisomycin (activator). Cell viability, cytokine expression, and ERK/p38 MAPK phosphorylation were assessed.
Results: SH improved nasal symptoms, reduced epithelial injury, and normalized nasal pH in ARS rats. It downregulated IL-1β, IL-6, TNF-α, and ICAM-1 while upregulating IL-4. Transmission electron microscopy showed restoration of ciliary and mitochondrial integrity. In HNEpCs, 60 μM SH was optimal by CCK-8 assay. In LPS-stimulated cells, SH suppressed IL-1β/IL-6 mRNA and inhibited ERK and p38 MAPK phosphorylation; these effects were reversed by Anisomycin, confirming pathway involvement.
Conclusion: SH alleviates sinonasal inflammation in ARS by inhibiting bacterial activity and restoring epithelial integrity through p38 MAPK/ERK suppression. These findings support SH as a potential therapy for upper airway inflammatory diseases.
Keywords: sodium houttuyfonate, acute rhinosinusitis, houttuynia cordata, p38 MAPK/ERK signaling, inflammation, ethnopharmacology