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

机译：吸入氢气衰减过敏性哮喘小鼠的气道炎症和氧化应激

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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. 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. 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. 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.
机译：哮喘是一个全球常见的慢性气道疾病，不能治愈并导致公共卫生的巨额负担。氧化应激被认为是哮喘发病机制的重要机制。已经证明了氢气作为一种新的抗氧化剂，并且在许多疾病中施加治疗性抗氧化活性，并且这种无毒气体在哮喘中的功能尚不清楚。该研究的目的旨在研究吸入氢气对哮喘小鼠模型的病理生理学的影响。本研究使用了卵磷蛋白（OVA）诱导的过敏气道炎症的鼠模型。简而言之，小鼠致溶于卵亮官，并分别在OVA或PBS攻击后连续7天每天吸入67％的氢气60Ω分钟。在具有4个生物信号系统通道的装置中评估肺功能。通过H / E和周期性酸性孢子染色染色形态和脚酚细胞增生。通过Wright Giemsa染色分析了支气管肺泡灌洗液（BALF）中的细胞学分类。收集血清，BALF和肺组织进行生化测定。单向分析方差（ANOVA）用于确定组之间的统计学意义。通过使用GraphPad Prism 5软件，Bonferroni的多个比较测试进行了多种比较。吸入氢气消毒卵泡 - 诱导肺抗性的增加。同时，哮喘小鼠显示出严重的炎症性浸润和戈尔特细胞增生，其被氢气吸入逆转。氢气吸入显着降低了BALF中总细胞，嗜酸性粒细胞和淋巴细胞的数量。吸入后，BALF和IL-4中的IL-4，IL-13，TNF-α和CXCL15水平的增加程度显着下降。氢气吸入明显上调过量脂肪酶降低的活性，并显着减弱了丙二醛和髓氧化酶的增加。氢气吸入改善肺功能并保护建立的气道炎症在过敏性哮喘模型中，这可能与氧化应激过程的抑制相关。本研究为哮喘的临床管理提供了潜在的替代治疗机会。

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