Asthma is a chronic, serious allergic inflammatory disease in the airway. The inflammation in the airway is induced by the allergic T-helper 2 cells (Th2 cells), which leads to unfettered production of inflammatory cytokines. The accretion of inflammatory cells in the airway also speeds up the secretion of reactive oxygen species (ROS) and suppresses antioxidative processes. Hence, the present work aimed to study the antiasthmatic efficacy of betulin and its effect in suppressing the inflammatory markers of ovalbumin (OVA) challenged asthmatic mice. The observed results revealed that the levels of inflammatory cells including neutrophils, eosinophils, lymphocytes, and macrophages were effectively decreased by betulin treatment; furthermore, the inflammatory markers IL-4, IL-5, IL-13, and TNF-α levels were notably suppressed by betulin administration in OVA-challenged asthmatic mice. Similarly, the oral administration of betulin showed a reduction in IgE level and elevation in the IFN-γ level in bronchoalveolar lavage fluid (BALF). The elevated levels of antioxidant enzymes like catalase (CAT), glutathione (GSH), and superoxide dismutase (SOD) were observed in betulin treated mice. Furthermore, reduced levels of reactive oxygen species like NO₂, NO₃, and MDA were noted in the betulin treated group. Consistently, airway hyperreactivity (AHR) was depleted in the betulin administered group compared with the OVA-challenged asthmatic group. Betulin treatment was revealed to have noteworthy antiasthmatic effects mediated by the suppression of production of inflammatory cells and the expression of other inflammatory markers. Furthermore, the elevation in the level of antioxidant markers helped to disclose the original regulatory mode of betulin on asthma treatment.

中文翻译：

---

桦木素对卵子诱发的哮喘小鼠炎症生物标志物和氧化状态的影响。

哮喘是气道中的一种慢性，严重的过敏性炎症性疾病。气道中的炎症是由过敏性T-helper 2细胞（Th2细胞）诱导的，导致炎症细胞因子的产生不受限制。气道中炎性细胞的积聚还可以加快活性氧（ROS）的分泌并抑制抗氧化过程。因此，本工作旨在研究白蛋白的抗哮喘功效及其在抑制卵清蛋白（OVA）攻击的哮喘小鼠炎症标记中的作用。观察结果表明，通过白桦蛋白治疗可有效降低包括中性粒细胞，嗜酸性粒细胞，淋巴细胞和巨噬细胞在内的炎症细胞的水平。此外，炎症标志物IL-4，IL-5，IL-13，在患有OVA的哮喘小鼠中，白桦蛋白给药可显着抑制TNF-α和TNF-α的水平。类似地，口服白桦蛋白在支气管肺泡灌洗液（BALF）中显示IgE水平降低和IFN-γ水平升高。在用贝特林治疗的小鼠中观察到抗氧化酶（如过氧化氢酶（CAT），谷胱甘肽（GSH）和超氧化物歧化酶（SOD））水平升高。此外，减少了活性氧的含量，例如NO在贝特林治疗组中注意到₂，NO ₃和MDA。一致地，与经OVA攻击的哮喘组相比，白桦林给药组的气道高反应性（AHR）减少了。揭示了通过抑制炎性细胞的产生和其他炎性标志物的表达介导的贝特林治疗具有显着的抗哮喘作用。此外，抗氧化剂标记物水平的提高有助于揭示白桦蛋白对哮喘治疗的原始调节方式。