Magnesium hydride ameliorates endotoxin-induced acute respiratory distress syndrome by inhibiting inflammation, oxidative stress, and cell apoptosis
Shi X, Zhu L, Wang S, Zhu W, Li Q, Wei J, Feng D, Liu M, Chen Y, Sun X, Lu H, Lv X. · Oxidative Medicine and Cellular Longevity. 2022;2022:5918954.
Study at a glance
Preclinical
Male C57BL/6 mice exposed to intraperitoneal or intratracheal lipopolysaccharide and A549 alveolar epithelial cells exposed to LPS.
Mice received oral MgH₂ 50 mg/kg daily for three days before LPS; cells received 500 μM MgH₂ after a concentration screen. · MgH₂ dose was 50 mg/kg/day in mice and 500 μM in cell experiments. The amount, concentration and time course of released molecular H₂ were not measured.
Three days of preventive oral dosing before endotoxin; survival followed for three days after lethal-dose LPS, with shorter tissue/cell assays.
All LPS-only mice in the lethal model died within three days, while reported survival with MgH₂ was nearly 40%. Lung injury/edema, inflammatory and oxidative markers, apoptosis and barrier-protein changes favored MgH₂ in both models. Mg(OH)₂ did not reproduce the reported effect. Cell viability showed no significant change below 500 μM MgH₂; no clinical endpoint was studied.
Pre-treatment rather than rescue therapy, lethal endotoxin models that do not reproduce all ARDS biology, A549 cancer-derived cells, animal sample sizes absent from the main report and actual H₂ exposure unmeasured. Chinese public/institutional grants supported the work; authors declared no commercial or financial conflicts.
What kind of evidence is this?
Preclinical
Preventive oral-treatment experiments in two mouse endotoxin lung-injury models plus LPS-stimulated A549-cell experiments
Respiratory health
H₂-rich water
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
Male C57BL/6 mice exposed to intraperitoneal or intratracheal lipopolysaccharide and A549 alveolar epithelial cells exposed to LPS.
The article does not report a consolidated animal total or per-group n in the methods/main figure text; this missing sample-size information is retained explicitly.
Three days of preventive oral dosing before endotoxin; survival followed for three days after lethal-dose LPS, with shorter tissue/cell assays.
Mice received oral MgH₂ 50 mg/kg daily for three days before LPS; cells received 500 μM MgH₂ after a concentration screen.
H₂ generated chemically in the stomach or cell medium when MgH₂ reacts with water — not Brown's gas, not inhaled H₂ and not H₂-rich drinking water.
MgH₂ dose was 50 mg/kg/day in mice and 500 μM in cell experiments. The amount, concentration and time course of released molecular H₂ were not measured.
Saline control, LPS alone and equimolar-magnesium Mg(OH)₂ control in mice; untreated/LPS and N-acetylcysteine conditions in cells.
Outcomes and reported result
Survival, lung histology/injury score and wet:dry ratio, BALF cytokines, oxidative markers, apoptosis/tight-junction proteins and AKT/mTOR/NF-κB/NLRP3 pathway measures.
All LPS-only mice in the lethal model died within three days, while reported survival with MgH₂ was nearly 40%. Lung injury/edema, inflammatory and oxidative markers, apoptosis and barrier-protein changes favored MgH₂ in both models. Mg(OH)₂ did not reproduce the reported effect. Cell viability showed no significant change below 500 μM MgH₂; no clinical endpoint was studied.
The complete free PMC article, methods, figures, supplement descriptions and disclosures were checked for preventive timing, both models, MgH₂/Mg(OH)₂ dosing, missing animal counts and released-H₂ measurement, positive/null findings, funding and conflicts.
A reported association, difference or mechanism is not automatically a clinical benefit.
Limitations and applicability
Pre-treatment rather than rescue therapy, lethal endotoxin models that do not reproduce all ARDS biology, A549 cancer-derived cells, animal sample sizes absent from the main report and actual H₂ exposure unmeasured. Chinese public/institutional grants supported the work; authors declared no commercial or financial conflicts.
Preventive MgH₂ exposure in mice/cells; it does not establish treatment, dose or safety in people with ARDS.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
PMID: 35528515 · DOI: 10.1155/2022/5918954
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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