Inhalation of hydrogen gas attenuates airway inflammation and oxidative stress in allergic asthmatic mice.

Asthma research and practice Pub Date : 2018-03-15 eCollection Date: 2018-01-01 DOI:10.1186/s40733-018-0040-y
Ning Zhang, Changwen Deng, Xingxing Zhang, Jingxi Zhang, Chong Bai
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引用次数: 32

Abstract

Background: Asthma is a worldwide common chronic airway disease that cannot be cured and results in the huge burden in public health. Oxidative stress was considered an important mechanism in the pathogenesis of asthma. Hydrogen gas been demonstrated to function as a novel antioxidant and exert therapeutic antioxidant activity in a number of diseases and the function of this nontoxic gas in asthma was unclear. The purpose of the study aims to examine the effect of inhalation hydrogen gas on the pathophysiology of a mouse model of asthma.

Methods: A murine model of ovalbumin (OVA)-induced allergic airway inflammation was used in this study. Briefly, Mice were sensitized to ovalbumin and received inhalation of 67% high concentration of hydrogen gas for 60 min once a day for 7 consecutive days after OVA or PBS challenge respectively. Lung function was assessed in the apparatus with 4 channels of biological signal system. Morphology and goblet cell hyperplasia were stained by H/E and Periodic acid-Schiff staining. Cytologic classification in the bronchial alveolar lavage fluid (BALF) was analyzed by Wright Giemsa staining. Serum, BALF and lung tissue were collected for biochemical assay. One-way analysis of variance (ANOVA) was used to determine statistical significance between groups. Multiple comparisons were made by Bonferroni's Multiple Comparison Test by using GraphPad Prism 5 software.

Results: Inhalation of hydrogen gas abrogated ovalbumin-induced the increase in lung resistance. Concomitantly, the asthmatic mice showed severe inflammatory infiltration and goblet cell hyperplasia which were reversed by hydrogen gas inhalation. Hydrogen gas inhalation reduced significantly the number of total cells, eosinophils and lymphocytes in BALF. Increased level of IL-4, IL-13, TNF-α and CXCL15 in the BALF and IL-4 in the serum were decreased significantly after inhalation. Hydrogen gas inhalation markedly upregulated the activity of decreased superoxide dismutase and significantly attenuated the increased level of malondialdehyde and myeloperoxidase.

Conclusions: Hydrogen gas inhalation improves lung function and protects established airway inflammation in the allergic asthmatic mice model which may be associated with the inhibition of oxidative stress process. This study provides a potential alternative therapeutic opportunity for the clinical management of asthma.

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吸入氢气可减轻过敏性哮喘小鼠气道炎症和氧化应激。
背景:哮喘是一种世界范围内常见的无法治愈的慢性气道疾病,给公共卫生造成了巨大负担。氧化应激被认为是哮喘发病的重要机制。氢气已被证明是一种新型抗氧化剂,并在许多疾病中发挥治疗性抗氧化活性,但这种无毒气体在哮喘中的作用尚不清楚。本研究旨在探讨吸入氢气对哮喘小鼠模型病理生理的影响。方法:采用卵清蛋白(OVA)致小鼠变应性气道炎症模型。简单地说,小鼠对卵清蛋白致敏,分别在OVA或PBS刺激后,每天1次吸入高浓度67%的氢气,持续60分钟,连续7天。采用四通道生物信号系统评价肺功能。H/E染色和周期性酸-希夫染色观察形态学和杯状细胞增生情况。用Wright Giemsa染色法分析支气管肺泡灌洗液(BALF)的细胞学分类。采集血清、BALF和肺组织进行生化检测。采用单因素方差分析(ANOVA)确定组间的统计学显著性。采用GraphPad Prism 5软件,采用Bonferroni多重比较检验进行多重比较。结果:吸入氢气消除卵清蛋白可引起肺阻力增加。同时,哮喘小鼠表现出严重的炎症浸润和杯状细胞增生,吸入氢气可逆转这一现象。吸入氢气可显著降低BALF细胞总数、嗜酸性粒细胞和淋巴细胞数量。吸入后血清BALF中IL-4、IL-13、TNF-α、CXCL15水平升高,IL-4水平明显降低。吸入氢气可显著上调降低的超氧化物歧化酶活性,显著减弱丙二醛和髓过氧化物酶升高的水平。结论:吸入氢气可改善变应性哮喘小鼠肺功能,保护气道炎症,这可能与抑制氧化应激过程有关。本研究为哮喘的临床治疗提供了一个潜在的替代治疗机会。
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
自引率
0.00%
发文量
6
审稿时长
20 weeks
期刊介绍: Asthma Research and Practice is the official publication of Interasma and publishes cutting edge basic, clinical and translational research in addition to hot topic reviews and debate articles relevant to asthma and related disorders (such as rhinitis, COPD overlapping syndrome, sinusitis). The journal has a specialized section which focusses on pediatric asthma research. Asthma Research and Practice aims to serve as an international platform for the dissemination of research of interest to pulmonologists, allergologists, primary care physicians and family doctors, ENTs and other health care providers interested in asthma, its mechanisms and comorbidities.
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