Hydrogen-rich saline ameliorated LPS-induced acute lung injury via autophagy inhibition through the ROS/AMPK/mTOR pathway in mice
Wang Y, Zhang J, Bo J, Wang X, Zhu J. · Experimental Biology and Medicine. 2019;244(9):721-727.
Study at a glance
Preclinical
Forty male C57BL/6 mice in an intratracheal lipopolysaccharide acute-lung-injury model, with MLE-12 cell experiments.
H₂-rich saline 10 mL/kg intraperitoneally one hour before intratracheal LPS; cell culture medium was replaced with H₂-rich medium one hour before LPS. · H₂ was dissolved for six hours at 0.4 MPa, prepared within 24 hours and measured at an average 0.86 mmol/L.
Pretreatment one hour before LPS; mice were killed 12 hours later, while cell endpoints used article-specific intervals up to 24 hours.
H₂-rich saline/medium was associated with improved injury and oxidative/inflammatory measures and lower autophagy/AMPK activation. Total AMPK and total mTOR protein did not change significantly. The study tested pretreatment, not rescue after established acute lung injury.
Small short-term preclinical prevention model, nonclinical surrogate endpoints, unclear exact per-group mouse allocation, and pathway inference based partly on pharmacologic inhibitors in cells. Authors reported no financial support and declared no conflicts.
What kind of evidence is this?
Preclinical
Randomized five-group mouse experiment plus controlled mouse lung-cell assays
Respiratory health
Other forms
Information not yet classified
Some editorial classification fields are still pending. The source-reported outcomes and result are shown below; Hydrogenology does not infer a positive or negative signal from prose automatically.
Methods
Forty male C57BL/6 mice in an intratracheal lipopolysaccharide acute-lung-injury model, with MLE-12 cell experiments.
40 mice randomized among control, saline, LPS, H₂-rich saline plus LPS, and 3-methyladenine plus LPS groups. The text does not explicitly state equal per-group allocation; cell assays report three independent experiments.
Pretreatment one hour before LPS; mice were killed 12 hours later, while cell endpoints used article-specific intervals up to 24 hours.
H₂-rich saline 10 mL/kg intraperitoneally one hour before intratracheal LPS; cell culture medium was replaced with H₂-rich medium one hour before LPS.
H₂ dissolved in saline or cell-culture medium — H₂ only, not Brown's gas.
H₂ was dissolved for six hours at 0.4 MPa, prepared within 24 hours and measured at an average 0.86 mmol/L.
Control/saline, LPS injury and autophagy-inhibitor 3-methyladenine groups; mechanistic cell comparisons also used NAC and compound C.
Outcomes and reported result
Lung histology, wet/dry ratio, MDA, bronchoalveolar protein and inflammatory cells, cell viability/ROS, autophagy markers and AMPK/mTOR signaling.
H₂-rich saline/medium was associated with improved injury and oxidative/inflammatory measures and lower autophagy/AMPK activation. Total AMPK and total mTOR protein did not change significantly. The study tested pretreatment, not rescue after established acute lung injury.
The complete free PMC article was checked for animal groups, H₂ preparation/concentration, dose and timing, in-vivo and cell results, a reported null molecular result, funding and conflict declaration.
A reported association, difference or mechanism is not automatically a clinical benefit.
Limitations and applicability
Small short-term preclinical prevention model, nonclinical surrogate endpoints, unclear exact per-group mouse allocation, and pathway inference based partly on pharmacologic inhibitors in cells. Authors reported no financial support and declared no conflicts.
Acute LPS lung injury in mice/cells; it does not establish treatment of human ARDS or sepsis.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
PMID: 31042074 · DOI: 10.1177/1535370219847941
Free full article in PubMed Central.
Complete PMC article and PubMed metadata; full-text extraction checked 9 August 2026.
10 August 2026
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