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<p>Asthma is a chronic respiratory disease characterized by airway hyper-responsiveness, inflammation, and pulmonary edema. Asthma may be triggered by allergens, certain medications, environmental exposure, respiratory infection, and physical exertion. Patients with asthma express higher levels of T helper cell 2 (Th2) cytokines i.e., IL-4 and IL-5. Estragole (EST), a phytochemical in essential oils, has shown anti-inflammatory and immunomodulatory effects. Current study was set out with the objectives to evaluate the anti-asthmatic effects of EST using various in vivo and in vitro experiments. Thirty-six (36) albino <i>BALB/c</i> mice were divided into six groups: Normal group (NG), OVA-induced asthma group (DG), Methylprednisolone group (MPG group, 15&#xa0;mg/kg), Low, medium and high doses of EST (LDE: 10, 30 and 60&#xa0;mg/kg, respectively). Mice were sensitized with 20&#xa0;µg of OVA intraperitoneally and treated with EST during the challenge phase (21–27&#xa0;days). Lung wet/dry ratio, total and differential leukocyte counts (TLC and DLC) in blood and Bronchoalveolar Lavage fluid (BALF) collections, histopathology (H&amp;E, PAS), mRNA expressions of IL-4 and IL-5 in the lungs were analyzed, and molecular docking was performed. Airway inflammation was found ameliorated in EST treated groups as evident by reduction in TLC and DLC in both blood and BALF samples, and attenuation of infiltration of inflammatory cells in lungs. Furthermore, EST significantly reduced IL-4 and IL-5 mRNA expression levels in the lungs tissue and demonstrated notable binding affinity with IL-4 (− 4.5&#xa0;kcal/mol), IL-5 (− 4.7&#xa0;kcal/mol), and GATA-3 (− 5.3&#xa0;kcal/mol). These docking results support the in vivo findings by suggesting a possible interaction of EST with key Th2 mediators, and their transcriptional regulator to suppress downstream airway inflammation, consistent with its observed anti-asthmatic effects. Estragole possesses anti-asthmatic property by attenuation of airway inflammation and pulmonary edema. Molecular docking, RT-qPCR, and histopathological evaluations suggesting that EST may attenuate allergic asthma via attenuation in Th2-mediated markers i.e., IL-4, IL-5, and GATA-3.</p>

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Estragole protects against ovalbumin-induced allergic asthma by amelioration of interleukin-4 and interleukin-5 expression in BALB/c mice

  • 期刊论文

  • 发表日期：

    2025年11月4日

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  • Ashna Asim,
  • Arham Shabbir,
  • Urooj Alam,
  • Aisha Mobashar,
  • Sajida Parveen,
  • Tabinda Fatima,
  • Esraa M. Haji,
  • Ali F. Almutairy,
  • Sulaiman Mohammed Abdullah Alnasser,
  • Eid Fahad Alanazi,
  • Ashfaq Ahmad

摘要

Asthma is a chronic respiratory disease characterized by airway hyper-responsiveness, inflammation, and pulmonary edema. Asthma may be triggered by allergens, certain medications, environmental exposure, respiratory infection, and physical exertion. Patients with asthma express higher levels of T helper cell 2 (Th2) cytokines i.e., IL-4 and IL-5. Estragole (EST), a phytochemical in essential oils, has shown anti-inflammatory and immunomodulatory effects. Current study was set out with the objectives to evaluate the anti-asthmatic effects of EST using various in vivo and in vitro experiments. Thirty-six (36) albino BALB/c mice were divided into six groups: Normal group (NG), OVA-induced asthma group (DG), Methylprednisolone group (MPG group, 15 mg/kg), Low, medium and high doses of EST (LDE: 10, 30 and 60 mg/kg, respectively). Mice were sensitized with 20 µg of OVA intraperitoneally and treated with EST during the challenge phase (21–27 days). Lung wet/dry ratio, total and differential leukocyte counts (TLC and DLC) in blood and Bronchoalveolar Lavage fluid (BALF) collections, histopathology (H&E, PAS), mRNA expressions of IL-4 and IL-5 in the lungs were analyzed, and molecular docking was performed. Airway inflammation was found ameliorated in EST treated groups as evident by reduction in TLC and DLC in both blood and BALF samples, and attenuation of infiltration of inflammatory cells in lungs. Furthermore, EST significantly reduced IL-4 and IL-5 mRNA expression levels in the lungs tissue and demonstrated notable binding affinity with IL-4 (− 4.5 kcal/mol), IL-5 (− 4.7 kcal/mol), and GATA-3 (− 5.3 kcal/mol). These docking results support the in vivo findings by suggesting a possible interaction of EST with key Th2 mediators, and their transcriptional regulator to suppress downstream airway inflammation, consistent with its observed anti-asthmatic effects. Estragole possesses anti-asthmatic property by attenuation of airway inflammation and pulmonary edema. Molecular docking, RT-qPCR, and histopathological evaluations suggesting that EST may attenuate allergic asthma via attenuation in Th2-mediated markers i.e., IL-4, IL-5, and GATA-3.