Hydrogenology
Hydrogenology editorial study record

Molecular hydrogen protects against ischemia-reperfusion injury in a mouse fatty-liver model via regulating HO-1 and Sirt1 expression

Li S et al. · Sci Rep. 2018;8:14019.

PreclinicalOther formsPublished 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

Controlled mouse fatty-liver ischemia-reperfusion experiment plus primary-cell hypoxia-reoxygenation experiments

Research topic

Liver health

Administration classification

Other forms

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

Mice with diet-induced fatty liver and isolated hepatocytes and Kupffer cells

Sample

Principal animal figures report 5–7 mice per group; cell experiments used triplicate independent comparisons

Duration

15 minutes of ischemia and 3 hours of reperfusion in the principal animal experiment

Intervention

Hydrogen-rich saline containing 7 ppm H₂ during ischemia-reperfusion; cell experiments used H₂-treated culture conditions

Hydrogen form

H₂ dissolved in saline for the animal intervention and H₂-treated medium for cells — not Brown’s gas and not inhalation by the animals.

H₂ specification

7 ppm dissolved H₂ in saline for the in-vivo intervention.

H₂ flow

Not applicable to the animal treatment — saline administration, not inhalation. Cell-treatment gas flow is not reported in mL/min.

O₂ delivered with H₂

No O₂ was co-delivered as part of the animal H₂-saline intervention.

Comparator

Fatty-liver ischemia-reperfusion without H₂ and corresponding cell controls

Reported, not endorsed

Outcomes and reported result

Outcomes measured

Necrosis, macrophage infiltration, oxidative stress, apoptosis, AST, ALT, cytokines, HO-1 and Sirt1 signaling

Reported result

The article reports less liver injury, macrophage activation, inflammation and apoptosis and higher HO-1 and Sirt1-related measures with H₂ treatment.

Results-extraction completeness

Concentration, main methods, figures, conflicts and principal results checked in the open-access full text.

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 fatty-liver model with short reperfusion, small groups and separate cell experiments. Several authors were affiliated with the company MiZ.

Applies directly to

Diet-induced fatty liver ischemia-reperfusion in mice and isolated cells, not human liver surgery.

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: 30232347 · DOI: 10.1038/s41598-018-32411-4

Publisher access

Open-access full text is available through PMC and Scientific Reports.

Extraction basis

Open-access PMC/publisher full text and PubMed record.

Record revision

2026-08-10