Hydrogenology
Hydrogenology editorial study record

Hydrogen-rich saline attenuates brain injury induced by cardiopulmonary bypass and inhibits microvascular endothelial cell apoptosis via the PI3K/Akt/GSK3β signaling pathway in rats

Chen K et al. · Cell Physiol Biochem. 2017;43(4):1634–1647.

PreclinicalOther formsPublished 2017
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

Rat cardiopulmonary-bypass dose experiment with cerebral-microvascular-endothelial-cell mechanistic work

Research topic

Critical care and ischemia-reperfusion

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

Sprague-Dawley rats after experimental cardiopulmonary bypass and cultured rat cerebral microvascular endothelial cells

Sample

Animal and cell group sizes are not stated as a single total in the accessible article sections

Duration

Principal animal outcomes at 24 hours after bypass

Intervention

Hydrogen-rich saline 1, 4 or 6 mL/kg after cardiopulmonary bypass; 6 mL/kg was used in subsequent experiments

Hydrogen form

H₂ dissolved in saline — H₂ only, not Brown’s gas and not inhalation.

H₂ specification

0.8 mmol/L dissolved H₂; dose response at 1, 4 and 6 mL/kg. Administration route is not clearly stated in the extracted article text.

H₂ flow

Not applicable — saline administration, not gas inhalation; preparation flow was not reported.

O₂ delivered with H₂

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

Comparator

Sham and bypass controls, plus PI3K-pathway-inhibitor comparisons in cells

Reported, not endorsed

Outcomes and reported result

Outcomes measured

Neurological score, histology, blood-brain-barrier permeability, inflammatory and brain-injury markers, apoptosis and PI3K/Akt/GSK3β signaling

Reported result

The article reports the largest protection at 6 mL/kg, with lower injury, permeability, inflammation and apoptosis measures; pathway-inhibitor experiments were used to probe mechanism.

Results-extraction completeness

Open publisher article checked for preparation, concentration, dose response, timing and principal outcomes; total allocation and route remain unresolved.

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 bypass model with several doses and extensive pathway work; the article’s direction of some Akt/GSK3β findings requires cautious interpretation.

Applies directly to

Cardiopulmonary-bypass brain injury in rats and hypoxic endothelial cells, not cardiac-surgery outcomes in people.

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: 29040978 · DOI: 10.1159/000484024

Publisher access

Free full text is available at the publisher.

Extraction basis

Free publisher full text and PubMed record; no retraction or expression of concern was shown in the checked records on 7 August 2026.

Record revision

2026-08-10