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<p>Allergic asthma, the most common phenotype of asthma, is a chronic inflammatory airway disease driven by Type 2 immune responses and characterized by eosinophilic infiltration, elevated IgE levels, and activation of inflammatory pathways. This study investigated the anti-inflammatory and immunomodulatory effects of <i>Perilla frutescens</i> var. <i>acuta</i> Kudo extract (PFE), a plant rich in rosmarinic acid (RA), using an ovalbumin (OVA)-induced mouse model of allergic asthma. Given RA’s well-documented anti-allergic properties, extraction conditions were optimized to maximize RA yield. PFE treatment significantly reduced immune cell infiltration in bronchoalveolar lavage fluid, suppressed Th2-associated cytokine production, and decreased serum IgE levels, thereby alleviating airway inflammation. Mechanistically, PFE inhibited activation of NF-κB and p38 MAPK pathways, key drivers of inflammatory responses in allergic asthma. These findings suggest that PFE attenuates allergic airway inflammation through both immune regulation and suppression of pro-inflammatory signaling, supporting its potential as a natural therapeutic agent for allergic asthma.</p>

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Perilla frutescens Britton var. acuta Kudo ameliorates OVA-induced allergic asthma via inhibiting NF-κB and p38 signaling pathways

  • 期刊论文

  • 发表日期：

    2025年8月22日

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  • Juwon Choi,
  • Eun Bi Yoo,
  • Jooyoun Park,
  • Ardina Nur Fauziah,
  • Heeju Kim,
  • Minha Oh,
  • Minseok Kang,
  • Young Jun Kim,
  • Ji Yeon Kim,
  • Hong Jin Lee,
  • Sung Keun Jung,
  • Sung-Wook Hong,
  • Sanguine Byun

摘要

Allergic asthma, the most common phenotype of asthma, is a chronic inflammatory airway disease driven by Type 2 immune responses and characterized by eosinophilic infiltration, elevated IgE levels, and activation of inflammatory pathways. This study investigated the anti-inflammatory and immunomodulatory effects of Perilla frutescens var. acuta Kudo extract (PFE), a plant rich in rosmarinic acid (RA), using an ovalbumin (OVA)-induced mouse model of allergic asthma. Given RA’s well-documented anti-allergic properties, extraction conditions were optimized to maximize RA yield. PFE treatment significantly reduced immune cell infiltration in bronchoalveolar lavage fluid, suppressed Th2-associated cytokine production, and decreased serum IgE levels, thereby alleviating airway inflammation. Mechanistically, PFE inhibited activation of NF-κB and p38 MAPK pathways, key drivers of inflammatory responses in allergic asthma. These findings suggest that PFE attenuates allergic airway inflammation through both immune regulation and suppression of pro-inflammatory signaling, supporting its potential as a natural therapeutic agent for allergic asthma.