Echinacoside alleviates airway remodeling and inflammation in an ovalbumin-induced neonatal mouse model of asthma by modulating the SIRT1–NF-κB pathway

• Yunbo Pan ^[1] ; Yijun Liu ^[1]
  1. [1] Chongqing Medical University

     Chongqing Medical University

     China

     
• Localización: Allergologia et immunopathologia: International journal for clinical and investigate allergology and clinical immunology, ISSN-e 1578-1267, ISSN 0301-0546, Vol. 51, Nº. 4, 2023, págs. 71-77
• Idioma: inglés
• Texto completo no disponible (Saber más ...)
• Resumen

  • Purpose: Echinacoside (ECH) has been reported to have anti-inflammatory and anti-immune effects, and may be effective for treating asthma. This study aimed to investigate the effect of ECH on asthma.

    Methods: A mouse model of asthma was established by ovalbumin (OVA) induction, and the effect of ECH on airway remodeling in mice was evaluated using the Periodic Acid-Schiff stain and enzyme-linked immunosorbent serologic assay (ELISA). Additionally, the effect of ECH on collagen deposition in asthmatic mice was assessed using Western blotting (WB) analysis, and response to airway inflammation was evaluated by ELISA. The signaling pathway regulated by ECH was also investigated using WB.

    Results: Our findings demonstrated that ECH restored OVA-induced increase in mucin, -immunoglobulin E, and respiratory resistance. ECH also alleviated OVA-induced collagen -deposition, including collagen I, collagen III, alpha smooth muscle actin, and epithelial (E)-cadherin. Moreover, ECH restored the elevated levels of interleukin (IL)-13, IL-17, and the increased -number of macrophages, eosinophils, lymphocytes, and neutrophills induced by OVA. ECH mainly exerted its regulatory effects by modulating the silent mating type information regulation 2 homolog 1 (Sirtuin 1/SIRT1)–nuclear factor kappa B (NF-κB) signaling pathway in the mouse models of asthma.

    Conclusion: This study highlights the therapeutic potential of ECH for attenuating airway remodeling and inflammation in an OVA-induced neonatal mouse model of asthma through the modulation of SIRT1/NF-κB pathway.