Thiruvengadam Rekha, Govindarasu Mydhili, Khaled Jamal Mohammed Ali, Lee Seungho, Kim Jin Hee
Centre for Global Health Research-Helix Research Lab, Department of Neonatology, Saveetha Medical College and Hospital, Saveetha Institute of Medical and Technical Sciences (SIMATS), Saveetha University, Chennai, 600077, India.
Department of Integrative Bioscience & Biotechnology, Institute of Bioscience, Sejong University, Seoul 05006, Republic of Korea.
Int J Med Sci. 2025 Jul 24;22(13):3429-3438. doi: 10.7150/ijms.96371. eCollection 2025.
This study aimed to evaluate the anti-inflammatory effects of alpha-bisabolol (AB) in allergic airway inflammation-induced rat pups. We evaluated the anti-adverse effects of AB against allergic airway inflammation-induced male Wistar rat pups, with four categorized groups including vehicle-controls (group 1), controls treated with 25 mg/kg of AB (group 2), allergic airway inflammation-induced cases (group 3), and cases treated with 25 mg/kg of AB before allergic airway inflammation induction (group 4). Lung histopathology, bronchoalveolar lavage fluid eosinophils, and several inflammatory markers were also examined in each group. AB significantly decreased mucous gland hypertrophy, eosinophil infiltration, and oxidative stress marker levels in the allergic airway inflammation-induced AB-pretreated rats. Moreover, AB pretreatment significantly reduced the levels of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, IL-8, IL-17, monocyte chemoattractant protein-1, C-X-C chemokine receptor type 4 (CXCR4), and thymic stromal lymphopoietin, which were increased in allergic airway inflammation-induced cases. Furthermore, transcription of , , , , , and were significantly suppressed in allergic airway inflammation-induced AB-pretreated rats. These results indicate that AB can protect against neonatal asthma by inhibiting acute or chronic inflammation induced during disease onset.
本研究旨在评估α-红没药醇(AB)对过敏性气道炎症诱导的幼鼠的抗炎作用。我们评估了AB对过敏性气道炎症诱导的雄性Wistar幼鼠的抗不良影响,分为四个组,包括赋形剂对照组(第1组)、用25 mg/kg AB治疗的对照组(第2组)、过敏性气道炎症诱导的病例组(第3组)以及在过敏性气道炎症诱导前用25 mg/kg AB治疗的病例组(第4组)。还对每组进行了肺组织病理学、支气管肺泡灌洗液嗜酸性粒细胞以及几种炎症标志物的检查。在过敏性气道炎症诱导的AB预处理大鼠中,AB显著降低了黏液腺肥大、嗜酸性粒细胞浸润和氧化应激标志物水平。此外,AB预处理显著降低了促炎细胞因子的水平,如白细胞介素(IL)-1β、IL-6、IL-8、IL-17、单核细胞趋化蛋白-1、C-X-C趋化因子受体4(CXCR4)和胸腺基质淋巴细胞生成素,这些因子在过敏性气道炎症诱导的病例中有所增加。此外,在过敏性气道炎症诱导的AB预处理大鼠中, 、 、 、 、 和 的转录显著受到抑制。这些结果表明,AB可以通过抑制疾病发作期间诱导的急性或慢性炎症来预防新生儿哮喘。