Hydrogen ameliorates pulmonary hypertension in rats by anti-inflammatory and antioxidant effects.
Yasuaki Kishimoto, Taichi Kato, Mikako Ito, Yoshiteru Azuma, Yoshie Fukasawa, Kinji Ohno, Seiji Kojima · The Journal of thoracic and cardiovascular surgery · 2015
Research-use notice
Independent study record
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H2HUBB TAKEAWAY
This preclinical study evaluated molecular hydrogen in rats. 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 the researchers therefore hypothesized that molecular hydrogen would improve monocrotaline (MCT)-induced PAH in rats.
How Molecular Hydrogen Was Used
Nineteen male Sprague-Dawley rats (body weight: 200-300 g) were divided into groups, receiving: (1) MCT + hydrogen-saturated water (group H); (2) MCT + dehydrogenized water (group M); or (3) saline + dehydrogenized water (group C).
What the Researchers Found
Pulmonary arterial hypertension was significantly exacerbated in group M compared to group C, but was significantly improved in group H. Vascular density was significantly reduced in group M, but not in group H. Adventitial macrophages, antiproliferating cell nuclear antigen – and 8-OHdG-positive cells, and stromal cell-derived factor-1 and monocyte chemoattractant protein-1 expressions were significantly increased in group M, but improved in group H. Expressions of phosphorylated STAT3 and NFAT were up-regulated in group M, but improved in group H.
H₂ Mechanisms / Biological Findings
Molecular hydrogen ameliorates MCT-induced PAH in rats by suppressing macrophage accumulation, reducing oxidative stress and modulating the STAT3/NFAT axis. Beneficial effects of molecular hydrogen, which exerts both anti-inflammatory and antioxidative effects, have been reported for various pathologic conditions.
Authors’ Conclusion
The authors concluded that molecular hydrogen ameliorates MCT-induced PAH in rats by suppressing macrophage accumulation, reducing oxidative stress and modulating the STAT3/NFAT axis.