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Preclinical animal evidenceAnimal studyOther or not reported

Hydrogen‐rich saline reducing cardiac toxicity induced by adriamycin in rats (850.6)

Songqing Liu, Yunjia Liu, Pan Yu, Xuejun Sun · The FASEB Journal · 2014

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Research-use notice

Independent study record

Each H2HUBB study page organizes source-linked research details for educational use. Interpretation should remain proportional to the study design, population, controls, and limitations.

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Primary topic Cardiovascular Health
Evidence type Preclinical animal evidence
Publication type Animal study
Hydrogen method Other or not reported

H2HUBB TAKEAWAY

In rats, rats in the H₂ group displayed a reduced degree of myocardial neutrophilic infiltrate, necrosis, hemorrhage, and spindle‐shaped interstitial cells as compared with rats in the Control group. The number of TUNEL‐positive cells were increased in the myocardium in the Physiologic saline group and Control group. These results are preclinical and suggest molecular hydrogen's therapeutic potential in the condition studied. Further human research is needed to establish clinical effectiveness.

What the Researchers Studied

The study examined rats.

How Molecular Hydrogen Was Used

Physiologic saline, hydrogenrich Saline or nothing was administered through intraperitoneal (i.p.) injection after exposure to ADR (2.5 mg/kg/week for 6 weeks) respectively.

What the Researchers Found

Rats in the H₂ group displayed a reduced degree of myocardial neutrophilic infiltrate, necrosis, hemorrhage, and spindle‐shaped interstitial cells as compared with rats in the Control group..The number of TUNEL‐positive cells were increased in the myocardium in the Physiologic saline group and Control group. H₂ comparably decreased the frequency of TUNEL‐positive cells relative to the Control group. And the level of 8‐OHdG, IL‐1b and TNF‐a were decreased in the hydrogenrich Saline group.

H₂ Mechanisms / Biological Findings

The results of this study demonstrate that hydrogen‐rich saline ameliorated cardiotoxicity induced by Adriamycin by reducing oxidative stress and inflammatory cascades in heart tissue.

Authors’ Conclusion

A distinct authors’ conclusion was not available in the source material reviewed by H2HUBB.

CONTINUE EXPLORING

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