Abstract
Objective: Oxidative stress was considered an important mechanism in the pathogenesis of asthma. Hydrogen (H2) has 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. This study aims to examine the effect of H2 inhalation on the pathophysiology of a mice model of asthma.
Methods: A ovalbumin (OVA)-induced asthmatic mice model received inhalation of high concentration H2 for 60 min once a day for 7 consecutive days after OVA or PBS challenge respectively. Lung function, morphology and goblet cell hyperplasia were assessed. BALF, serum and lung tissue were collected for biochemical assay.
Results: Inhalation of H2 abrogated ovalbumin-induced the increase in lung resistance. The asthmatic mice showed severe inflammatory infiltration and goblet cell hyperplasia which were reversed by H2 inhalation. H2 inhalation reduced significantly the number of total cells, eosinophils and lymphocytes in bronchial alveolar lavage fluid. 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. H2 inhalation markedly upregulated the activity of decreased superoxide dismutase and significantly attenuated the increased level of malondialdehyde and myeloperoxidase.
Conclusions: H2 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 method for the clinical management of asthma.
- Copyright ©the authors 2017
