Hydrogen gas inhalation protects against cigarette smoke-induced COPD development in mice.

Background: Chronic obstructive pulmonary disease (COPD) is a chronic lung disease with limited treatment options. Hydrogen (H-2) has been shown to be anti-oxidative and anti-inflammatory. This study aimed to evaluate the beneficial effects of H-2 inhalation on COPD development in mice. Methods: A COPD mouse model was established in male C57BL mice by cigarette smoke (CS) exposure. The H-2 intervention was administered by atomisation inhalation. Lung functions were assessed by using Buxco lung function measurement system. The inflammatory cells were counted and the levels of IL-6 and KC in BALF were assayed with ELISA. The lung tissue was subjected to H&E or PAS or Masson's trichrome stain. Furthermore, 16HBE cells were used to evaluate the effects of H-2 on signaling change caused by hydrogen peroxide (H2O2)center dot H2O2 was used to treat 16HBE cells with or without H-2 pretreatment. The IL-6 and IL-8 levels in cell culture medium were measured. The levels of phosphorylated ERK1/2 and nucleic NF-kappa B in lungs and 16HBE cells were determined. Results: H-2 ameliorated CS-induced lung function decline, emphysema, inflammatory cell infiltration, small-airway remodelling, goblet-cell hyperplasia in tracheal epithelium and activated ERK1/2 and NF-kappa B in mouse lung. In 16HBE airway cells, H2O2 increased IL-6 and IL-8 secretion in conjunction with ERK1/2 and NF-kappa B activation. These changes were reduced by H-2 treatment. Conclusions: These findings demonstrated that H-2 inhalation could inhibit CS-induced COPD development in mice, which is associated with reduced ERK 1/2 and NE-kappa B-dependent inflammatory responses.