Allergic asthma is a chronic inflammatory disease characterized by airflow obstruction, airway hyperresponsiveness (AHR), airway inflammation, and mucus overproduction. Cordyceps polysaccharide (CPS) is one of the main bioactive compounds of Cordyceps militarisis, a traditional Chinese medicine. In this study, we established a mouse model of asthma using ovalbumin (OVA) challenge and evaluated the potential regulatory effect of CPS (25, 50, and 100 mg/kg) on asthmatic mice. These results showed that the asthmatic mice treated with CPS suppressed the secretion of eotaxin, IL-4, IL-5, IL-13, and IFN-γ in the blood and bronchoalveolar lavage fluid (BALF), and decreased serum IgE levels compared to the vehicle-treated mice. CPS also alleviated inflammatory cell infiltration, goblet cell hyperplasia, and the increases of inflammatory cells in the mouse model of asthma. In addition, OVA-induced AHR was inhibited by CPS treatment. Further analyses of protein expression revealed that CPS inhibited the activation of transforming growth factor β1 (TGF-β1)/Smad pathway in mice with asthma. These findings indicated that CPS might serve as a potential therapeutic agent for the management of allergic asthma.

中文翻译：

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虫草多糖通过 TGF-β1/Smad 信号通路改善卵清蛋白诱导的哮喘小鼠模型的气道炎症。

过敏性哮喘是一种慢性炎症性疾病，其特征是气流阻塞、气道高反应性 (AHR)、气道炎症和粘液过度产生。冬虫夏草多糖（CPS）是传统中药蛹虫草的主要生物活性化合物之一。在本研究中，我们使用卵清蛋白 (OVA) 激发建立了哮喘小鼠模型，并评估了 CPS（25、50 和 100 mg/kg）对哮喘小鼠的潜在调节作用。这些结果表明，与 CPS 相比，CPS 治疗的哮喘小鼠抑制了血液和支气管肺泡灌洗液 (BALF) 中嗜酸性粒细胞趋化因子、IL-4、IL-5、IL-13 和 IFN-γ 的分泌，并降低了血清 IgE 水平。载体处理的小鼠。CPS 还减轻了炎症细胞浸润、杯状细胞增生、以及哮喘小鼠模型中炎症细胞的增加。此外，CPS 治疗抑制了 OVA 诱导的 AHR。对蛋白质表达的进一步分析表明，CPS 抑制了哮喘小鼠中转化生长因子 β1 (TGF-β1)/Smad 通路的激活。这些发现表明，CPS 可能作为治疗过敏性哮喘的潜在治疗剂。