超声雾化递送的白芷外泌体样纳米囊泡缓解过敏性鼻炎并调节NF-κB信号通路
Angelica dahurica Exosome-like Nanovesicles Delivered by Ultrasonic Nebulization Alleviate Allergic Rhinitis and Modulate NF-κB Signaling.
文献信息
| PMID | 42797368 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Anqi Zhou |
| 作者单位 | State Key Laboratory of Biobased Material and Green Papermaking, School of Bioengineering, Qilu University of Technology (Shandong Academy of Sciences), Jinan 250353, China. |
| 期刊 | Pharmaceutics |
| SCI 分区 | Q1 |
| IF | 6.7 |
| 研究类型 | 基础研究 · 基础／转化 |
| 所属专科 | 鼻科 |
中文摘要
背景： 目前过敏性鼻炎（AR）的治疗伴有副作用，且不能提供确定性治愈。白芷具有公认的抗炎活性；然而，白芷来源的外泌体样纳米囊泡（ADELNs）在AR中的治疗潜力仍未被充分探索。此外，尽管超声雾化广泛用于气道炎症性疾病，包括肺部疾病和哮喘，但其在AR中的应用受到的关注有限。
方法： 通过差速离心和超速离心分离ADELNs，并使用透射电子显微镜（TEM）、纳米颗粒跟踪分析（NTA）、动态光散射（DLS）、薄层色谱（TLC）、SDS-PAGE和琼脂糖凝胶电泳进行表征。为评估超声雾化ADELNs对AR的作用，我们设计并验证了一种小鼠鼻腔雾化装置。随后建立细胞炎症和OVA诱导的AR小鼠模型，并使用ELISA、RT-qPCR、组织学染色及相关检测评估炎症和病理指标。采用蛋白质印迹法研究NF-κB信号通路的参与情况。
结果： ADELNs被成功分离，并表现出典型的外泌体样特征。超声雾化装置显示出良好的稳定性。雾化ADELNs以浓度依赖性方式缓解小鼠AR症状，降低炎性细胞因子、血清组胺和OVA特异性IgE，下调鼻黏膜中炎性细胞因子mRNA表达，改善鼻黏膜厚度，并减少肥大细胞浸润。为探索潜在机制，ADELN治疗与IκB和p65磷酸化降低以及NF-κB核转位减少相关，提示调节NF-κB信号可能有助于ADELNs的抗炎作用。
结论： 本研究成功分离并表征了ADELNs。使用自行设计的超声雾化装置进行小鼠鼻腔递送，我们表明ADELNs在体外抑制细胞炎症，缓解AR小鼠的症状和病理损伤，并可能通过抑制NF-κB信号通路发挥抗AR作用。这些发现为AR治疗提供了一种新策略。
英文摘要
Background: Current treatments for allergic rhinitis (AR) are associated with side effects and do not provide a definitive cure. Angelica dahurica has recognized anti-inflammatory activity; however, the therapeutic potential of Angelica dahurica-derived exosome-like nanovesicles (ADELNs) in AR remains insufficiently explored. In addition, although ultrasonic nebulization is widely used for airway inflammatory diseases, including pulmonary disorders and asthma, its application in AR has received limited attention. Methods: ADELNs were isolated by differential centrifugation and ultracentrifugation and characterized using transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), dynamic light scattering (DLS), thin-layer chromatography (TLC), SDS-PAGE, and agarose gel electrophoresis. To evaluate the effects of ultrasonic nebulized ADELNs on AR, we designed and validated a mouse nasal nebulization device. Cellular inflammation and OVA-induced AR mouse models were then established, and inflammatory and pathological indicators were assessed using ELISA, RT-qPCR, histological staining, and related assays. Western blotting was used to investigate the involvement of the NF-κB signaling pathway. Result: ADELNs were successfully isolated and exhibited typical exosome-like characteristics. The ultrasonic nebulization device showed good stability. Nebulized ADELNs alleviated AR symptoms in mice in a concentration-dependent manner, reduced inflammatory cytokines, serum histamine, and OVA-specific IgE, downregulated inflammatory cytokine mRNA expression in the nasal mucosa, improved nasal mucosal thickness, and decreased mast cell infiltration. To explore the potential mechanism, ADELN treatment was associated with reduced IκB and p65 phosphorylation and decreased NF-κB nuclear translocation, suggesting that modulation of NF-κB signaling may contribute to the anti-inflammatory effects of ADELNs. Conclusions: This study successfully isolated and characterized ADELNs. Using a self-designed ultrasonic nebulization device for mouse nasal delivery, we showed that ADELNs inhibited cellular inflammation in vitro, alleviated symptoms and pathological injury in AR mice, and may exert anti-AR effects by suppressing the NF-κB signaling pathway. These findings provide a new strategy for AR treatment.