Hydrogen-rich saline pretreatment significantly attenuated cigarette smoke-induced airway mucus production, goblet cell hyperplasia, and epithelial damage in rats through free radical scavenging mechanisms and modulation of EGFR and Nrf2 signaling pathways. These findings suggest that hydrogen therapy may have therapeutic potential for treating abnormal mucus production in COPD and other chronic airway diseases. This represents the first demonstration that intraperitoneal hydrogen-rich saline administration can protect airways against cigarette smoke-induced damage.
Plain-Language Summary
Researchers exposed rats to cigarette smoke to study how it damages airways, then tested whether hydrogen-rich saline (a salt solution containing dissolved hydrogen) could reduce the damage. They found that hydrogen-rich saline reduced mucus buildup, prevented excessive mucus-producing cells from forming, and protected airway tissue by neutralizing harmful molecules called free radicals that cigarette smoke creates.
Abstract
Over-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. Male 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. Hydrogen-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. Hydrogen-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.
