Hydrogen-rich solution attenuates myocardial injury caused by cardiopulmonary bypass in rats via the JAK2/STAT3 signaling pathway
Chen K, Sun Y, Diao Y, Zhang T, Dong W. · Oncology Letters. 2018;16(1):167–178.
What kind of evidence is this?
Preclinical
Randomized three-group rat cardiopulmonary-bypass experiment plus neonatal-rat cardiomyocyte hypoxia/reoxygenation experiments
Cardiovascular and circulatory health
Other forms
Not reported in this record.
Not reported in this record.
Methods at a glance
Adult male Sprague-Dawley rats undergoing thoracotomy or 60-minute cardiopulmonary bypass, plus cultured neonatal-rat cardiomyocytes.
30 adult rats randomized to sham, bypass or bypass plus H₂-rich solution, n=10 per group; neonatal cardiomyocytes were obtained from offspring, but one consolidated cell-experiment replicate count was not reported.
Injection three days before bypass; 60-minute bypass and in-vivo collection at 24 hours; cell hypoxia for two hours followed by four hours of reoxygenation.
One intraperitoneal injection of H₂-rich physiological solution, 6 mL/kg, three days before bypass; cultured cardiomyocytes received H₂-rich solution around hypoxia/reoxygenation and JAK2-siRNA manipulations.
H₂ dissolved in physiological solution — H₂ only, not Brown's gas and not inhalation.
Dose was 6 mL/kg. The article says the solution was prepared by pressurization according to a previous report but does not state its numeric H₂ concentration or preparation flow.
Not applicable — injected/culture solution, not gas inhalation; preparation flow was not reported.
No O₂ was co-delivered as part of the H₂ intervention.
Sham thoracotomy and bypass without H₂-rich solution; cell controls included hypoxia/reoxygenation, control siRNA and JAK2 siRNA groups.
Outcomes and reported result
Myocardial histology/fibrosis, cytokines, cTnI, hFABP, SOD, MDA, MPO, apoptosis/cell viability and JAK2/STAT3-related proteins.
Histology and all prespecified serum injury, inflammatory and oxidative markers favored H₂ solution versus bypass alone; cell viability/apoptosis and pathway markers also changed in the reported protective direction. JAK2 knockdown alone did not significantly change several cell outcomes and attenuated multiple H₂-associated effects.
The complete free PMC article, figures and methods were checked for allocation, route/dose, missing concentration/flow, in-vivo and cell findings including null comparisons, funding and conflicts.
A reported association, difference or mechanism is not automatically a clinical benefit. Null findings, outcome type, study design and precision all matter.
Cautions and applicability
Preclinical prophylactic timing, small male-rat groups, unreported H₂ concentration, broad mechanistic outcome set and incomplete cell-replicate reporting. Chinese national, Liaoning and university grants funded the work; authors declared no competing interests.
Rat bypass injury and cultured cardiomyocytes; it does not establish perioperative benefit or dosing in people.
Not reported in this record.
Not reported in this record.
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.
Sources and record status
PMID: 29928398 · DOI: 10.3892/ol.2018.8639
Free full article in PubMed Central.
Complete PMC article and PubMed metadata; full-text extraction checked 9 August 2026.
2026-08-10