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<p>β-Glucan (β-Glu), a bioactive macromolecular polysaccharide known for its immunomodulatory properties, was employed as a nanoparticle carrier to enhance the delivery of budesonide (BUD) in acute bronchial asthma treatment. This study evaluated budesonide- encapsulated β-glucan nanoparticles (BUD@β-Glu NPs) prepared via ionic gelation, which had an average size of 127.6 ± 1.32&#xa0;nm, a zeta potential of 3.3 ± 0.13 mV, and an 86.7 ± 2.4% encapsulation efficiency. A cumulative release of 72.5% of the drug was achieved after 24&#xa0;h. In vitro cytocompatibility of BUD@β-Glu NPs was assessed on L929 fibroblast cells using CCK-8 assay. It exhibited remarkable biocompatibility, as indicated by the high cell viability (&gt; 90%) in all groups at 24&#xa0;h. Using an ovalbumin-induced asthma mouse model, treatment with BUD@β-Glu NPs significantly decreased pro-inflammatory cytokines (IL-4, IL-5, TNF-α) and downregulated p38 MAPK phosphorylation by 65%, indicating effective suppression of airway inflammation. Histological analysis revealed reduced epithelial thickening and mucus production. Notably, BUD@β-Glu NPs increase adherence to nebulizer therapy and reduce airway inflammation in acute bronchial asthma by modulating cytokine signaling. These findings highlight the need for optimized nursing strategies to monitor and enlighten patients on proficient drug delivery systems.</p> Graphical Abstract <p></p>

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Fabrication of Budesonide-Encapsulated β-Glucan Nanoparticles for Alleviation of Acute Bronchial Asthma via Modulation of the p38 MAPK Signaling Pathway

  • 期刊论文

  • 发表日期：

    2026年5月28日

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  • Hongxia Gu,
  • Yangyang Fan,
  • Yunlei Ma,
  • Huiting Hu,
  • Xiangyan Yu

摘要

β-Glucan (β-Glu), a bioactive macromolecular polysaccharide known for its immunomodulatory properties, was employed as a nanoparticle carrier to enhance the delivery of budesonide (BUD) in acute bronchial asthma treatment. This study evaluated budesonide- encapsulated β-glucan nanoparticles (BUD@β-Glu NPs) prepared via ionic gelation, which had an average size of 127.6 ± 1.32 nm, a zeta potential of 3.3 ± 0.13 mV, and an 86.7 ± 2.4% encapsulation efficiency. A cumulative release of 72.5% of the drug was achieved after 24 h. In vitro cytocompatibility of BUD@β-Glu NPs was assessed on L929 fibroblast cells using CCK-8 assay. It exhibited remarkable biocompatibility, as indicated by the high cell viability (> 90%) in all groups at 24 h. Using an ovalbumin-induced asthma mouse model, treatment with BUD@β-Glu NPs significantly decreased pro-inflammatory cytokines (IL-4, IL-5, TNF-α) and downregulated p38 MAPK phosphorylation by 65%, indicating effective suppression of airway inflammation. Histological analysis revealed reduced epithelial thickening and mucus production. Notably, BUD@β-Glu NPs increase adherence to nebulizer therapy and reduce airway inflammation in acute bronchial asthma by modulating cytokine signaling. These findings highlight the need for optimized nursing strategies to monitor and enlighten patients on proficient drug delivery systems.

Graphical Abstract