Abstract
BackgroundOver-production of mucus is an important pathophysiological feature in chronic airway disease such as chronic obstructive pulmonary disease (COPD) and asthma. Cigarette smoking (CS) is the leading cause of COPD. Oxidative stress plays a key role in CS-induced airway abnormal mucus production. Hydrogen protected cells and tissues against oxidative damage by scavenging hydroxyl radicals. In the present study we investigated the effect of hydrogen on CS-induced mucus production in rats.MethodsMale Sprague-Dawley rats were divided into four groups: sham control, CS group, hydrogen-rich saline pretreatment group and hydrogen-rich saline control group. Lung morphology and tissue biochemical changes were determined by immunohistochemistry, Alcian Blue/periodic acid-Schiff staining, TUNEL, western blot and realtime RT-PCR.ResultsHydrogen-rich saline pretreatment attenuated CS-induced mucus accumulation in the bronchiolar lumen, goblet cell hyperplasia, muc5ac over-expression and abnormal cell apoptosis in the airway epithelium as well as malondialdehyde increase in the BALF. The phosphorylation of EGFR at Tyr1068 and Nrf2 up-regulation expression in the rat lungs challenged by CS exposure were also abrogated by hydrogen-rich saline.ConclusionHydrogen-rich saline pretreatment ameliorated CS-induced airway mucus production and airway epithelium damage in rats. The protective role of hydrogen on CS-exposed rat lungs was achieved at least partly by its free radical scavenging ability. This is the first report to demonstrate that intraperitoneal administration of hydrogen-rich saline protected rat airways against CS damage and it could be promising in treating abnormal airway mucus production in COPD.
Highlights
Chronic obstructive pulmonary disease (COPD) has become a major global epidemic that is increasing throughout the world, in developing countries [1]
Abnormal mucus production is recognized as a key pathophysiological feature in chronic obstructive pulmonary disease (COPD), including those without cough and sputum production and it should be a therapeutic target for all COPD subjects [3]
After four consecutive weeks of repeated cigarette smoke exposure, bronchiolar lumen obstruction by mucus and cell debris, and inflammatory cell infiltration were observed in the lumen of lungs from rats in the Cigarette smoking (CS) exposure group
Summary
Chronic obstructive pulmonary disease (COPD) has become a major global epidemic that is increasing throughout the world, in developing countries [1]. Goblet cell hyperplasia and excessive mucus production causes airway obstruction, which contributes to the morbidity and mortality of this disease [2]. Abnormal mucus production is recognized as a key pathophysiological feature in COPD, including those without cough and sputum production and it should be a therapeutic target for all COPD subjects [3]. Oxidative stress increased in COPD patients [6] and chronic lung oxidative damage are key contributors to the pathogenesis of COPD, which includes mucus hypersecretion, heightened apoptosis and chronic inflammation [7]. Oxidative stress is considered to be an important therapeutic target in COPD [8]. Over-production of mucus is an important pathophysiological feature in chronic airway disease such as chronic obstructive pulmonary disease (COPD) and asthma. Oxidative stress plays a key role in CS-induced airway abnormal mucus production. In the present study we investigated the effect of hydrogen on CSinduced mucus production in rats
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