Effects of hydrogen-rich saline on early acute kidney injury in severely burned rats by suppressing oxidative stress induced apoptosis and inflammation.
Song-Xue Guo, Quan Fang, Chuan-Gang You, Yun-Yun Jin, Xin-Gang Wang, Xin-Lei Hu, Chun-Mao Han · Journal of translational medicine · 2015
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Independent study record
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H2HUBB TAKEAWAY
In Sprague-Dawley rats, the oxidation-reduction potential and malondialdehyde levels were markedly reduced with hydrogen-rich saline treatment, whereas endogenous antioxidant enzyme activities were significantly increased. 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
This study investigated the potential protective effects of hydrogen against severe burn-induced early AKI in rats.
How Molecular Hydrogen Was Used
Fifty-six Sprague-Dawley rats were randomly divided into Sham, Burn + saline, and Burn + hydrogen-rich saline (HS) groups, and renal function and the apoptotic index were measured.
What the Researchers Found
Renal function and tubular apoptosis were improved by HS treatment. The oxidation-reduction potential and malondialdehyde levels were markedly reduced with HS treatment, whereas endogenous antioxidant enzyme activities were significantly increased. HS also decreased the myeloperoxidase levels and influenced the release of inflammatory mediators in the sera and renal tissues of the burned rats. The regulatory effects of HS included the inhibition of p38, JNK, ERK and NF-κB activation, and an increase in Akt phosphorylation.
H₂ Mechanisms / Biological Findings
Hydrogen can attenuate severe burn-induced early AKI; the mechanisms of protection include the inhibition of oxidative stress induced apoptosis and inflammation, which may be mediated by regulation of the MAPKs, Akt and NF-κB signalling pathways.
Authors’ Conclusion
The authors concluded that hydrogen can attenuate severe burn-induced early AKI; the mechanisms of protection include the inhibition of oxidative stress induced apoptosis and inflammation, which may be mediated by regulation of the MAPKs, Akt and NF-κB signalling pathways.