Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Xiao-Feng Xuan-Qiao decoction alleviates allergic rhinitis by inhibiting neutrophil extracellular trap formation.
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Li Tao, Lin Lili, Wang Min, Xiong Yingcai, Wang Zhao, Pan Wei, Dou Yuzhu, Qin Mengxue, Zhao Xiangguang, Hu Menglong, Fan Huizi, Dai Qigang, Wang Shouchuan, Ji Jianjian, Cai Liangyu
Аннотация
BACKGROUND: Allergic rhinitis (AR) is a chronic inflammatory disorder of the nasal mucosa, mediated by immunoglobulin E (IgE), and represents a significant global public health concern. The management of AR frequently involves corticosteroid-based pharmacotherapy; however, long-term treatment often results in diminished efficacy and is associated with significant adverse effects. Traditional Chinese Medicine has demonstrated promising clinical efficacy in addressing allergic asthma while effectively circumventing these limitations. The Xiao Feng Xuan Qiao (XF) decoction, a traditional Chinese herbal formulation, has demonstrated notable clinical efficacy in managing AR, although its underlying mechanisms remain unclear.
PURPOSE: This study aimed to elucidate the potential mechanisms of XF in the treatment of AR.
METHODS: Pediatric blood transcriptomics, clinical data, and an ovalbumin-induced mouse model were used to evaluate the effects of XF. Clinical symptoms, immunologic responses, histopathology, and molecular mechanisms were analyzed using enzyme-linked immunosorbent assay, flow cytometry, transcriptomics, immunohistochemistry, and immunofluorescence.
RESULTS: The findings revealed that XF significantly ameliorated clinical symptoms in AR-induced mice, as evidenced by reductions in sneezing, nasal rubbing, and other allergic manifestations. Furthermore, XF lowered IgE levels and reduced the infiltration of eosinophils, neutrophils, and mast cells in the serum of AR-induced mice. Transcriptomic and functional analyses revealed that XF markedly inhibited neutrophil extracellular trap (NETosis) formation. Mechanistically, XF primarily suppressed the TLR2-ERK-PKC signaling pathway, thereby reducing reactive oxygen species production, thus preventing NETosis.
CONCLUSION: The results of this study provide a novel theoretical foundation for the application of XF in AR treatment.
PURPOSE: This study aimed to elucidate the potential mechanisms of XF in the treatment of AR.
METHODS: Pediatric blood transcriptomics, clinical data, and an ovalbumin-induced mouse model were used to evaluate the effects of XF. Clinical symptoms, immunologic responses, histopathology, and molecular mechanisms were analyzed using enzyme-linked immunosorbent assay, flow cytometry, transcriptomics, immunohistochemistry, and immunofluorescence.
RESULTS: The findings revealed that XF significantly ameliorated clinical symptoms in AR-induced mice, as evidenced by reductions in sneezing, nasal rubbing, and other allergic manifestations. Furthermore, XF lowered IgE levels and reduced the infiltration of eosinophils, neutrophils, and mast cells in the serum of AR-induced mice. Transcriptomic and functional analyses revealed that XF markedly inhibited neutrophil extracellular trap (NETosis) formation. Mechanistically, XF primarily suppressed the TLR2-ERK-PKC signaling pathway, thereby reducing reactive oxygen species production, thus preventing NETosis.
CONCLUSION: The results of this study provide a novel theoretical foundation for the application of XF in AR treatment.