Effect of Betulin on Inflammatory Biomarkers and Oxidative Status of Ova-Induced Murine Asthma.

IF 2.1 4区 医学 Q3 TOXICOLOGY
Lei Wang, Diansheng Zhong
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引用次数: 3

Abstract

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.

白桦素对ova诱导的小鼠哮喘炎症生物标志物和氧化状态的影响。
哮喘是气道中一种慢性、严重的过敏性炎症性疾病。气道炎症是由过敏性辅助性t - 2细胞(Th2细胞)诱导的,这导致炎症细胞因子的不受约束的产生。气道中炎症细胞的增加也会加速活性氧(ROS)的分泌并抑制抗氧化过程。因此,本研究旨在研究白桦素的平喘作用及其对卵清蛋白(OVA)激发哮喘小鼠炎症标志物的抑制作用。结果表明,白桦素可有效降低炎症细胞水平,包括中性粒细胞、嗜酸性粒细胞、淋巴细胞和巨噬细胞;此外,白桦素可显著抑制ova哮喘小鼠炎症标志物IL-4、IL-5、IL-13和TNF-α水平。同样,口服白桦素可降低支气管肺泡灌洗液(BALF)中IgE水平和升高IFN-γ水平。在白桦脂素处理的小鼠中,过氧化氢酶(CAT)、谷胱甘肽(GSH)和超氧化物歧化酶(SOD)等抗氧化酶水平升高。此外,白桦素处理组的活性氧如NO2、NO3和MDA水平降低。与ova挑战哮喘组相比,白桦素组气道高反应性(AHR)持续减少。研究发现,桦木素治疗通过抑制炎症细胞的产生和其他炎症标志物的表达而具有显著的平喘作用。此外,抗氧化标志物水平的升高有助于揭示白桦素对哮喘治疗的原始调节模式。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
20
审稿时长
>12 weeks
期刊介绍: The Journal of Environmental Pathology, Toxicology and Oncology publishes original research and reviews of factors and conditions that affect human and animal carcinogensis. Scientists in various fields of biological research, such as toxicologists, chemists, immunologists, pharmacologists, oncologists, pneumologists, and industrial technologists, will find this journal useful in their research on the interface between the environment, humans, and animals.
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