Hydrogenology
Hydrogenology editorial study record

Hydrogen inhalation improves mouse neurological outcomes after cerebral ischemia/reperfusion independent of anti-necroptosis

Huang JL, Liu WW, Sun XJ. · Medical Gas Research. 2018;8(1):1–5.

PreclinicalInhaled H₂Published 2018
Study record, not medical adviceThis page reports one source and Hydrogenology’s source-text extraction. It does not establish that molecular hydrogen is effective, safe or appropriate for any person. Human, animal and laboratory evidence must not be treated as equivalent.
Source and classification

What kind of evidence is this?

Evidence stream

Preclinical

Reported design

Randomized controlled mouse middle-cerebral-artery occlusion experiment

Research topic

Other neurological conditions

Administration classification

Inhaled H₂

Study result signal

Not reported in this record.

Outcome type

Not reported in this record.

Reported in the source

Methods at a glance

Population or model

C57BL mice with one hour of middle-cerebral-artery occlusion followed by reperfusion.

Sample

Assay-specific group sizes were n=8 for infarct ratio, n=5 for brain water, n=17–18 for neurological score and n=3–5 for molecular assays; the article does not provide one consolidated animal total.

Duration

Ninety minutes from the start of reperfusion; most outcomes at 24 hours, with MLKL time points through 72 hours.

Intervention

Beginning at reperfusion, mice inhaled the test gas for 90 minutes.

Hydrogen form

Brown's gas / oxyhydrogen — H₂ and O₂ co-generated by water electrolysis.

H₂ specification

66.7% H₂ and 33.3% O₂ from an AMS-H-01 hydrogen/oxygen nebulizer.

H₂ flow

Not reported — gas composition is given but total generator flow is absent, so H₂ mL/min cannot be calculated.

O₂ delivered with H₂

33.3% O₂ was co-delivered; O₂ flow in mL/min was not reported.

Comparator

A 66.7% N₂/33.3% O₂ gas control, plus untreated ischemia-reperfusion and sham groups.

Reported, not endorsed

Outcomes and reported result

Outcomes measured

Infarct ratio, brain water content, neurological deficit and MLKL protein/mRNA expression as a necroptosis-pathway measure.

Reported result

Infarct ratio was 20.21±4.43% with oxyhydrogen versus 39.51±5.30% with untreated ischemia-reperfusion and 34.83±3.53% with N₂/O₂ control. Brain water and neurological scores also favored oxyhydrogen. MLKL protein and mRNA were not changed by the intervention, so the proposed anti-necroptosis mechanism was not supported.

Results-extraction completeness

The complete free article, oxyhydrogen composition, assay-specific sample sizes, positive and null results, stated limitations, funding and conflict declaration were checked.

A reported association, difference or mechanism is not automatically a clinical benefit. Null findings, outcome type, study design and precision all matter.

Interpretation limits

Cautions and applicability

Design and reporting cautions

Preclinical short-term stroke model, assay-specific small groups, no consolidated animal total, no reported total gas flow, no functional follow-up beyond the acute period and mechanistic tests that were null. Chinese National Natural Science Foundation grants funded the work; authors declared no conflict of interest.

Applies directly to

Acute focal cerebral ischemia-reperfusion in mice; not evidence of treatment efficacy in people with stroke.

Preliminary appraisal framework

Not reported in this record.

Preliminary risk-of-bias status

Not reported in this record.

Appraisal rationale

Not reported in this record.

No single-study GRADE certainty rating is assigned. Certainty is assessed by important outcome across a complete eligible evidence set, not by attaching a final grade to one source.

Provenance

Sources and record status

Identifiers

PMID: 29770189 · DOI: 10.4103/2045-9912.229596

Publisher access

Open-access PubMed Central article.

Extraction basis

Complete PubMed Central article and PubMed metadata; full-text extraction checked 9 August 2026.

Record revision

2026-08-10