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氢气吸入可减轻卵清蛋白诱导的哮喘BALB/c小鼠模型的气道炎症和氧化应激。

Hydrogen Gas Inhalation Alleviates Airway Inflammation and Oxidative Stress on Ovalbumin-Induced Asthmatic BALB/c Mouse Model.

作者信息

He Wenjing, Rahman Md Habibur, Bajgai Johny, Abdul-Nasir Sofian, Mo Chaodeng, Ma Hui, Goh Seong Hoon, Bomi Kim, Jung Hyeran, Kim Cheol-Su, Lee Hyungdon, Lee Kyu-Jae

机构信息

Department of Convergence Medicine, Wonju College of Medicine, Yonsei University, Wonju 26426, Republic of Korea.

Department of Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju 26426, Republic of Korea.

出版信息

Antioxidants (Basel). 2024 Oct 30;13(11):1328. doi: 10.3390/antiox13111328.

DOI:10.3390/antiox13111328
PMID:39594470
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11591407/
Abstract

Airway inflammatory diseases, such as asthma, are a global public health concern owing to their chronic inflammatory effects on the respiratory mucosa. Molecular hydrogen (H) has recently been recognized for its antioxidant and anti-inflammatory properties. In this study, we examined the therapeutic potential of H in airway inflammation using an ovalbumin (OVA)-induced BALB/c mouse model of allergic asthma. Female BALB/c mice were sensitized and challenged with OVA to induce airway inflammation, and 30 mice were randomly divided into five groups: NT (non-treatment), HTC (3% H treatment only), NC (negative control, OVA only), PC (positive control, OVA + intranasal 1 mg/mL salbutamol 50 μL), and HT (H treatment, OVA + inhaled 3% H). Various inflammatory and oxidative stress (OS)-induced markers such as white blood cells (WBCs) and their differential counts, lung histology, cytokine levels such as interleukin (IL)-4, (IL)-5, (IL)-13, interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), granulocyte-macrophage colony-stimulating factor (GM-CSF), (IL)-10, reactive oxygen species (ROS), nitric oxide (NO), glutathione peroxidase (GPx), and catalase (CAT), and total immunoglobulin E (IgE) levels were investigated. Our results showed that inhaled H significantly reduced inflammatory cell infiltration, OS markers, and pro-inflammatory cytokine expression while upregulating antioxidant enzyme activity. Furthermore, H also significantly decreased serum IgE levels, a marker of allergic inflammation. Collectively, our findings suggest that H inhalation is a promising treatment option for airway inflammation, offering a novel approach with potential clinical applications.

摘要

气道炎性疾病,如哮喘,因其对呼吸道黏膜的慢性炎症作用而成为全球公共卫生问题。分子氢(H₂)最近因其抗氧化和抗炎特性而受到认可。在本研究中,我们使用卵清蛋白(OVA)诱导的BALB/c小鼠过敏性哮喘模型,研究了H₂在气道炎症中的治疗潜力。雌性BALB/c小鼠用OVA致敏并激发以诱导气道炎症,30只小鼠随机分为五组:NT(未治疗)、HTC(仅3% H₂治疗)、NC(阴性对照,仅OVA)、PC(阳性对照,OVA + 鼻内1 mg/mL沙丁胺醇50 μL)和HT(H₂治疗,OVA + 吸入3% H₂)。研究了各种炎症和氧化应激(OS)诱导的标志物,如白细胞(WBC)及其分类计数、肺组织学、细胞因子水平,如白细胞介素(IL)-4、(IL)-5、(IL)-13、干扰素-γ(IFN-γ)、肿瘤坏死因子-α(TNF-α)、粒细胞-巨噬细胞集落刺激因子(GM-CSF)、(IL)-10、活性氧(ROS)、一氧化氮(NO)、谷胱甘肽过氧化物酶(GPx)和过氧化氢酶(CAT),以及总免疫球蛋白E(IgE)水平。我们的结果表明,吸入H₂显著减少了炎症细胞浸润、OS标志物和促炎细胞因子表达,同时上调了抗氧化酶活性。此外,H₂还显著降低了血清IgE水平,这是过敏性炎症的一个标志物。总体而言,我们的研究结果表明,吸入H₂是气道炎症的一种有前景的治疗选择,提供了一种具有潜在临床应用的新方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/9d1b57256e01/antioxidants-13-01328-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/fc9358db474f/antioxidants-13-01328-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/1dbcc6e8ea83/antioxidants-13-01328-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/89dc5005e1f3/antioxidants-13-01328-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/b5bcf6edf0e5/antioxidants-13-01328-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/03ebe92137e2/antioxidants-13-01328-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/9d1b57256e01/antioxidants-13-01328-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/fc9358db474f/antioxidants-13-01328-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/1dbcc6e8ea83/antioxidants-13-01328-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/89dc5005e1f3/antioxidants-13-01328-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/b5bcf6edf0e5/antioxidants-13-01328-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/03ebe92137e2/antioxidants-13-01328-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3fb/11591407/9d1b57256e01/antioxidants-13-01328-g006.jpg

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