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.
Study at a glance
Preclinical
Sprague-Dawley rats after experimental cardiopulmonary bypass and cultured rat cerebral microvascular endothelial cells
Hydrogen-rich saline 1, 4 or 6 mL/kg after cardiopulmonary bypass; 6 mL/kg was used in subsequent experiments · 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.
Principal animal outcomes at 24 hours after bypass
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.
Preclinical bypass model with several doses and extensive pathway work; the article’s direction of some Akt/GSK3β findings requires cautious interpretation.
What kind of evidence is this?
Preclinical
Rat cardiopulmonary-bypass dose experiment with cerebral-microvascular-endothelial-cell mechanistic work
Critical care and ischemia-reperfusion
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
Sprague-Dawley rats after experimental cardiopulmonary bypass and cultured rat cerebral microvascular endothelial cells
Animal and cell group sizes are not stated as a single total in the accessible article sections
Principal animal outcomes at 24 hours after bypass
Hydrogen-rich saline 1, 4 or 6 mL/kg after cardiopulmonary bypass; 6 mL/kg was used in subsequent experiments
H₂ dissolved in saline — H₂ only, not Brown’s gas and not inhalation.
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.
Sham and bypass controls, plus PI3K-pathway-inhibitor comparisons in cells
Outcomes and reported result
Neurological score, histology, blood-brain-barrier permeability, inflammatory and brain-injury markers, apoptosis and PI3K/Akt/GSK3β signaling
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.
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.
Limitations and applicability
Preclinical bypass model with several doses and extensive pathway work; the article’s direction of some Akt/GSK3β findings requires cautious interpretation.
Cardiopulmonary-bypass brain injury in rats and hypoxic endothelial cells, not cardiac-surgery outcomes in people.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
PMID: 29040978 · DOI: 10.1159/000484024
Free full text is available at the publisher.
Free publisher full text and PubMed record; no retraction or expression of concern was shown in the checked records on 7 August 2026.
10 August 2026
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