Hydrogen Water Helps Prevent Lung Disease in Newborn Rats
- Authors
- Yukako Muramatsu, Mikako Ito, Takahiro Oshima, Seiji Kojima, Kinji Ohno
- Journal
- Pediatric Pulmonology
- Year
- 2016
- DOI
- 10.1002/ppul.23386
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Bronchopulmonary Dysplasia
- Body System
- Respiratory
TL;DR
Drinking hydrogen-rich water helped prevent lung damage in a rat model of a newborn lung disease called bronchopulmonary dysplasia (BPD).
Key Finding
In a rat model of bronchopulmonary dysplasia, hydrogen-rich water consumed during pregnancy reduced lung damage, decreased inflammatory markers, and normalized abnormal lung tissue enlargement in newborns exposed to bacterial toxins.
Summary
Researchers created a rat model of bronchopulmonary dysplasia (a lung development disorder in newborns caused by inflammation) by exposing fetuses to a bacterial toxin. Pregnant rats that drank hydrogen-rich water showed protection against lung damage in their offspring. Hydrogen reduced markers of cellular damage, lowered inflammatory proteins, and helped restore normal lung structure in the newborn rats.
Practical Takeaway
This is an early-stage animal study suggesting hydrogen-rich water may help protect against a specific type of lung injury in newborns. However, results from rat studies do not automatically translate to humans, and no human trials have tested this approach. Much more research, including human studies, would be needed before hydrogen-rich water could be considered a treatment for this condition.
Abstract
Bronchopulmonary dysplasia (BPD) is characterized by developmental arrest of the alveolar tissue. Oxidative stress is causally associated with development of BPD. The effects of hydrogen have been reported in a wide range of disease models and human diseases especially caused by oxidative stress. We made a rat model of BPD by injecting lipopolysaccharide (LPS) into the amniotic fluid at E16.5. The mother started drinking hydrogen-rich water from E9.5 and also while feeding milk. Hydrogen normalized LPS-induced abnormal enlargement of alveoli at P7 and P14. LPS increased staining for nitrotyrosine and 8-OHdG of the lungs, and hydrogen attenuated the staining. At P1, LPS treatment decreased expressions of genes for FGFR4, VEGFR2, and HO-1 in the lungs, and hydrogen increased expressions of these genes. In contrast, LPS treatment and hydrogen treatment had no essential effect on the expression of SOD1. Inflammatory marker proteins of TNFα and IL-6 were increased by LPS treatment, and hydrogen suppressed them. Treatment of A549 human lung adenocarcinoma epithelial cells with 10% hydrogen gas for 24 hr decreased production of reactive oxygen species in both LPS-treated and untreated cells. Lack of any known adverse effects of hydrogen makes hydrogen a promising therapeutic modality for BPD. Pediatr Pulmonol. 2016; 51:928-935. © 2016 Wiley Periodicals, Inc.