Hydrogen-rich saline demonstrates protective effects against lipopolysaccharide-induced pulmonary fibrosis and epithelial-to-mesenchymal transition through its selective hydroxyl radical scavenging properties and suppression of oxidative stress. The treatment significantly attenuated fibrotic markers, reversed loss of epithelial cell adhesion molecules, and restored antioxidant enzyme activity in lung tissues. These findings suggest hydrogen-rich saline may have therapeutic potential for preventing fibrotic complications in acute respiratory distress syndrome patients.
Plain-Language Summary
Researchers gave mice a lung injury using a bacterial toxin, then treated some with hydrogen-rich saline (salt water containing dissolved hydrogen gas). They found that hydrogen-rich saline reduced lung scarring and prevented the transformation of lung cells into scar-forming cells. The treatment also reduced harmful molecules called free radicals (unstable atoms that damage cells) and restored the lung's natural antioxidant defenses (the body's ability to neutralize these harmful molecules).
Abstract
Background Fibrotic change is one of the important reasons for the poor prognosis of patients with acute respiratory distress syndrome (ARDS). The present study investigated the effects of hydrogen-rich saline, a selective hydroxyl radical scavenger, on lipopolysaccharide (LPS)-induced pulmonary fibrosis. Material/Methods Male ICR mice were divided randomly into 5 groups: Control, LPS-treated plus vehicle treatment, and LPS-treated plus hydrogen-rich saline (2.5, 5, or 10 ml/kg) treatment. Twenty-eight days later, fibrosis was assessed by determination of collagen deposition, hydroxyproline, and type I collagen levels. Development of epithelial-to-mesenchymal transition (EMT) was identified by examining protein expressions of E-cadherin and α-smooth muscle actin (α-SMA). Transforming growth factor (TGF)-β1 content, total antioxidant capacity (T-AOC), malondialdehyde (MDA) content, catalase (CAT), and superoxide dismutase (SOD) activity were determined. Results Mice exhibited increases in collagen deposition, hydroxyproline, type I collagen contents, and TGF-β1 production in lung tissues after LPS treatment. LPS-induced lung fibrosis was associated with increased expression of α-SMA, as well as decreased expression of E-cadherin. In addition, LPS treatment increased MDA levels but decreased T-AOC, CAT, and SOD activities in lung tissues, indicating that LPS induced pulmonary oxidative stress. Hydrogen-rich saline treatment at doses of 2.5, 5, or 10 ml/kg significantly attenuated LPS-induced pulmonary fibrosis. LPS-induced loss of E-cadherin in lung tissues was largely reversed, whereas the acquisition of α-SMA was dramatically decreased by hydrogen-rich saline treatment. In addition, hydrogen-rich saline treatment significantly attenuated LPS-induced oxidative stress. Conclusions Hydrogen-rich saline may protect against LPS-induced EMT and pulmonary fibrosis through suppressing oxidative stress.
DOI: 10.12659/MSM.900452
